scholarly journals Effects of mild whole body hypothermia on self-paced exercise performance

2018 ◽  
Vol 125 (2) ◽  
pp. 479-485
Author(s):  
Steven A. H. Ferguson ◽  
Neil D. Eves ◽  
Brian D. Roy ◽  
Gary J. Hodges ◽  
Stephen S. Cheung

This study examined self-paced, high-intensity exercise during mild hypothermia and whether hyperoxia might offset any potential impairment. Twelve trained males each completed 15-km time trials in three environmental conditions: Neutral (23°C, [Formula: see text] 0.21), Cold (0°C, [Formula: see text] 0.21), and Cold+Hyper (0°C, [Formula: see text] 0.40). Cold and Cold+Hyper trials occurred after a 0.5°C drop in rectal temperature. Rectal temperature was higher ( P ≤ 0.016) throughout Neutral compared with Cold and Cold+Hyper; Cold had a higher ( P ≤ 0.035) rectal temperature than Cold+Hyper from 2.5 to 7.5 km, and hyperoxia did not alter thermal sensation or comfort. Oxyhemoglobin saturation decreased from ~98% to ~94% with Neutral and Cold, but was maintained at ~99% in Cold+Hyper ( P < 0.01). Cerebral tissue oxygenation index (TOI) was higher in Neutral than in Cold throughout the time trial (TT) ( P ≤ 0.001), whereas Cold+Hyper were unchanged ( P ≥ 0.567) from Neutral by 2.5 km. Muscle TOI was maintained in Cold+Hyper compared with Neutral and was higher ( P ≤ 0.046) than Cold throughout the entire TT. Power output during Cold (246 ± 41 W) was lower than Neutral (260 ± 38 W) at all 2.5-km intervals ( P ≤ 0.012) except at 12.5 km. Power output during Cold+Hyper (256 ± 42 W) was unchanged ( P ≥ 0.161) from Neutral throughout the TT, and was higher than Cold from 7.5 km onward. Average cadence was higher in Neutral (93 ± 8 rpm) than in either Cold or Cold+Hyper (Cold: 89 ± 7 and Cold+Hyper: 90 ± 8 rpm, P = 0.031). In conclusion, mild hypothermia reduced self-paced exercise performance; hyperoxia during mild hypothermia restored performance to thermoneutral levels, likely due to maintenance of oxygen availability rather than any thermogenic benefit. NEW & NOTEWORTHY We examined self-paced, high-intensity exercise with 0.5°C rectal temperature decreases in a 0°C ambient environment, along with whether hyperoxia could offset any potential impairment. During a 15-km time trial, power output was lower with hypothermia than with thermoneutral. However, with hypothermia, hyperoxia of [Formula: see text] = 0.40 restored power output despite there being no thermophysiological improvement. Hypothermia impairs exercise performance, whereas hyperoxia likely restored performance due to maintenance of oxygen availability rather than any thermogenic benefit.

Author(s):  
Lieke E. van Iersel ◽  
Yala R. Stevens ◽  
Jose M. Conchillo ◽  
Freddy J. Troost

Abstract Background Nutritional supplementation is commonly used by athletes to improve their exercise performance. Previous studies demonstrated that citrus flavonoid extract (CFE) supplementation may be an effective strategy to improve exercise performance in male athletes. Yet, no conclusive research has been performed to investigate the effect of chronic CFE supplementation on high-intensity exercise performance under anaerobic conditions. Therefore, the aim of the study was to assess whether CFE supplementation in daily dosages of 400 and 500 mg for a period of 4 and 8 weeks improves anaerobic exercise capacity. Methods A randomized, double-blind, placebo controlled, parallel clinical study was conducted in 92 moderately trained healthy men and women. Subjects were randomized to receive 400 mg of CFE (n = 30), 500 mg of CFE (n = 31) or placebo (n = 31) daily, for 8 consecutive weeks. The Wingate anaerobic test was used to assess anaerobic exercise capacity and power output at baseline, after 4 weeks and after 8 weeks. Results After 4 weeks supplementation, average power output significantly increased in the 400 mg group (Estimated difference [ED] = 38.2 W [18.0, 58.3]; p < 0.001; effect size [ES] = 0.27) and in the 500 mg group (ED = 21.2 W [0.91, 41.4]; p = 0.041; ES = 0.15) compared to placebo. The 5 s peak power output was also increased in the 400 mg group (ED = 53.6 [9.96, 97.2]; p = 0.017; ES = 0.25) after 4 weeks compared to placebo. After 8 weeks of supplementation, average power output was significantly improved in the group receiving 400 mg of CFE (ED = 31.6 [8.33, 54.8]; p = 0.008; ES = 0.22) compared to placebo. Conclusion These results demonstrate that CFE supplementation improved anaerobic capacity and peak power during high intensity exercise in moderately trained individuals. Further research is needed to identify the underlying mechanisms that are affected by CFE supplementation. Trial registration ClinicalTrials.gov (NCT03044444). Registered 7 February 2017


2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.


2019 ◽  
Vol 44 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Gary J. Hodges ◽  
Steven A.H. Ferguson ◽  
Stephen S. Cheung

This study examined the effect of mild hypothermia (a 0.5 °C decrease in rectal temperature) on heart rate variability (HRV), with the identical hypothermia protocol performed twice and compared using intraclass correlation coefficient (r) analysis to study the repeatability. Twelve healthy males each completed 1 neutral (23 °C) and 2 cold (0 °C) trials. In the neutral trial, participants sat quietly for 30 min. In the cold trials, baseline data were obtained from a 5-min sample following 30 min of quiet sitting at 23 °C, followed by passive exposure to 0 °C; hypothermic measures were taken from a 5-min period immediately prior to rectal temperature decreasing by 0.5 °C. HRV was obtained from a 3-lead electrocardiogram. There were no differences (all p > 0.05) in baseline measures between the neutral and the 2 cold trials, suggesting no precooling anxiety related to the cold trials. Heart rate, together with HRV measures (i.e., root mean square difference of successive normal RR intervals, triangular interpolation of NN interval histogram, low-frequency oscillations (LF), and high-frequency oscillations (HF)), increased (all p < 0.05) with mild hypothermia and showed excellent reliability between the 2 cold trials (all r ≥ 0.81). In contrast, the LF/HF ratio decreased (p < 0.05) and had only fair reliability between the 2 cold trials (r = 0.551). In general, hypothermia led to increases in heart rate, together with most measures of HRV. Although it was counterintuitive that both sympathetic and vagal influences would increase simultaneously, these changes likely reflected increased stress from whole-body cooling, together with marked cardiovascular strain and sympathetic nervous system activity from shivering to defend core body temperature. An important methodological consideration for future studies is the consistent and repeatable HRV responses to hypothermia.


2018 ◽  
Vol 315 (5) ◽  
pp. E1034-E1045 ◽  
Author(s):  
Kristoffer Svensson ◽  
Jessica R. Dent ◽  
Shahriar Tahvilian ◽  
Vitor F. Martins ◽  
Abha Sathe ◽  
...  

The pyruvate dehydrogenase complex (PDC) converts pyruvate to acetyl-CoA and is an important control point for carbohydrate (CHO) oxidation. However, the importance of the PDC and CHO oxidation to muscle metabolism and exercise performance, particularly during prolonged or high-intensity exercise, has not been fully defined especially in mature skeletal muscle. To this end, we determined whether skeletal muscle-specific loss of pyruvate dehydrogenase alpha 1 ( Pdha1), which is a critical subunit of the PDC, impacts resting energy metabolism, exercise performance, or metabolic adaptation to high-fat diet (HFD) feeding. For this, we generated a tamoxifen (TMX)-inducible Pdha1 knockout (PDHmKO) mouse, in which PDC activity is temporally and specifically ablated in adult skeletal muscle. We assessed energy expenditure, ex vivo muscle contractile performance, and endurance exercise capacity in PDHmKO mice and wild-type (WT) littermates. Additionally, we studied glucose homeostasis and insulin sensitivity in muscle after 12 wk of HFD feeding. TMX administration largely ablated PDHα in skeletal muscle of adult PDHmKO mice but did not impact energy expenditure, muscle contractile function, or low-intensity exercise performance. Additionally, there were no differences in muscle insulin sensitivity or body composition in PDHmKO mice fed a control or HFD, as compared with WT mice. However, exercise capacity during high-intensity exercise was severely impaired in PDHmKO mice, in parallel with a large increase in plasma lactate concentration. In conclusion, although skeletal muscle PDC is not a major contributor to resting energy expenditure or long-duration, low-intensity exercise performance, it is necessary for optimal performance during high-intensity exercise.


2006 ◽  
Vol 100 (1) ◽  
pp. 194-202 ◽  
Author(s):  
L. Havemann ◽  
S. J. West ◽  
J. H. Goedecke ◽  
I. A. Macdonald ◽  
A. St Clair Gibson ◽  
...  

The aim of this study was to investigate the effect of a high-fat diet (HFD) followed by 1 day of carbohydrate (CHO) loading on substrate utilization, heart rate variability (HRV), effort perception [rating or perceived exertion (RPE)], muscle recruitment [electromyograph (EMG)], and performance during a 100-km cycling time trial. In this randomized single-blind crossover study, eight well-trained cyclists completed two trials, ingesting either a high-CHO diet (HCD) (68% CHO energy) or an isoenergetic HFD (68% fat energy) for 6 days, followed by 1 day of CHO loading (8–10 g CHO/kg). Subjects completed a 100-km time trial on day 1 and a 1-h cycle at 70% of peak oxygen consumption on days 3, 5, and 7, during which resting HRV and resting and exercising respiratory exchange ratio (RER) were measured. On day 8, subjects completed a 100-km performance time trial, during which blood samples were drawn and EMG was recorded. Ingestion of the HFD reduced RER at rest ( P < 0.005) and during exercise ( P < 0.01) and increased plasma free fatty acid levels ( P < 0.01), indicating increased fat utilization. There was a tendency for the low-frequency power component of HRV to be greater for HFD-CHO ( P = 0.056), suggestive of increased sympathetic activation. Overall 100-km time-trial performance was not different between diets; however, 1-km sprint power output after HFD-CHO was lower ( P < 0.05) compared with HCD-CHO. Despite a reduced power output with HFD-CHO, RPE, heart rate, and EMG were not different between trials. In conclusion, the HFD-CHO dietary strategy increased fat oxidation, but compromised high intensity sprint performance, possibly by increased sympathetic activation or altered contractile function.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Avlant Nilsson ◽  
Elias Björnson ◽  
Mikael Flockhart ◽  
Filip J. Larsen ◽  
Jens Nielsen

Abstract Human muscles are tailored towards ATP synthesis. When exercising at high work rates muscles convert glucose to lactate, which is less nutrient efficient than respiration. There is hence a trade-off between endurance and power. Metabolic models have been developed to study how limited catalytic capacity of enzymes affects ATP synthesis. Here we integrate an enzyme-constrained metabolic model with proteomics data from muscle fibers. We find that ATP synthesis is constrained by several enzymes. A metabolic bypass of mitochondrial complex I is found to increase the ATP synthesis rate per gram of protein compared to full respiration. To test if this metabolic mode occurs in vivo, we conduct a high resolved incremental exercise tests for five subjects. Their gas exchange at different work rates is accurately reproduced by a whole-body metabolic model incorporating complex I bypass. The study therefore shows how proteome allocation influences metabolism during high intensity exercise.


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