Physical inactivity causes exercise resistance of fat metabolism: harbinger or culprit of disease?

Physical inactivity is the fourth leading cause of death in the world. It is associated with myriad diseases and premature death. Two possible contributing factors are postprandial lipidaemia (PPL), which accelerates atherosclerosis, and impaired whole-body fat oxidation, which contributes to obesity. Acute exercise in physically active people is effective for increasing whole body fat oxidation and lowering PPL the next morning. However, in people who have low physical activity (<8000 steps/day), an acute bout of exercise (1 h at 62% maximal oxygen consumption) has no effect on increasing fat oxidation or reducing PPL ('exercise resistance'). The acute harms of inactivity are not due to the lack of exercise and are more powerful than the benefits of exercise, at least regarding fat metabolism. The increase in mortality with reduced daily steps is remarkably steep. Low background steps/day also impair the metabolic adaptations to short-term endurance training, suggesting that the ills of inactivity extend beyond fat metabolism. 'Exercise resistance' with inactivity could be a culprit, causing atherosclerosis, or maybe also a harbinger (impaired fat oxidation) of more widespread diseases. Recommendations regarding the amount of moderate to vigorous exercise needed for health should factor in the amount of background activity (i.e. ∼8000 steps/day) necessary to avoid 'exercise resistance'.

Cardiovascular responses to hot skin at rest and during exercise.

Integrative cardiovascular responses to heat stress during endurance exercise depend on various variables, such as thermal stress and exercise intensity. This review addresses how increases in skin temperature alter and challenge the integrative cardiovascular system during upright submaximal endurance exercise, especially when skin is hot (i.e. >38°C). Current evidence suggests that exercise intensity plays a significant role in cardiovascular responses to hot skin during exercise. At rest and during mild intensity exercise, hot skin increases skin blood flow and abolishes cutaneous venous tone, which causes blood pooling in the skin while having little impact on stroke volume and thus cardiac output is increased with an increase in heart rate. When the heart rate is at relatively low levels, small increases in heart rate, skin blood flow, and cutaneous venous volume do not compromise stroke volume, so cardiac output can increase to fulfill the demands for maintaining blood pressure, heat dissipation, and the exercising muscle. On the contrary, during more intense exercise, hot skin does not abolish exercise-induced cutaneous venoconstriction possibly due to high sympathetic nerve activities; thus, it does not cause blood pooling in the skin. However, hot skin reduces stroke volume, which is associated with a decrease in ventricular filling time caused by an increase in heart rate. When the heart rate is high during moderate or intense exercise, even a slight reduction in ventricular filling time lowers stroke volume. Cardiac output is therefore not elevated when skin is hot during moderate intensity exercise.

Inactivity Causes Resistance to Improvements in Metabolism After Exercise.

Prolonged sitting prevents a 1-h bout of running from improving fat oxidation and reducing plasma triglycerides. This "exercise resistance" can be prevented by taking 8500 steps·d-1 or by interrupting 8 h of sitting with hourly cycle sprints. We hypothesize that there is an interplay between background physical activity (e.g., steps·d-1) and the exercise stimuli in regulating some acute and chronic adaptations to exercise.

Effects of short sprint interval training on aerobic and anaerobic indices: A systematic review and meta-analysis.

The effects of short sprint interval training (sSIT) with efforts of ≤10 s on maximal oxygen consumption (V̇O2 max), aerobic and anaerobic performances remain unknown. To verify the effectiveness of sSIT in physically active adults and athletes, a systematic literature search was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The databases PubMed/MEDLINE, ISI Web of Science, and SPORTDiscus were systematically searched on May 9, 2020, and updated on September 14, 2021. Inclusion criteria were based on PICO and included healthy athletes and active adults of any sex (≤40 years), performing supervised sSIT (≤10 s of "all-out" and non-"all-out" efforts) of at least 2 weeks, with a minimum of 6 sessions. As a comparator, a non-sSIT control group, another high-intensity interval training (HIIT) group, or a continuous training (CT) group were required. A total of 18 studies were deemed eligible. The estimated SMDs based on the random-effects model were -0.56 (95% CI: -0.79, -0.33, p < 0.001) for V̇O2 max, -0.43 (95% CI: -0.67, -0.20, p < 0.001) for aerobic performance, and -0.44 (95% CI: -0.70, -0.18, p < 0.001) for anaerobic performance after sSIT vs. no exercise/usual training. However, there were no significant differences (p > 0.05) for all outcomes when comparing sSIT vs. HIIT/CT. Our findings indicate a very high effectiveness of sSIT protocols in different exercise modes (e.g., cycling, running, paddling, and punching) to improve V̇O2 max, aerobic, and anaerobic performances in physically active young healthy adults and athletes.

Background Inactivity Blunts Metabolic Adaptations to Intense Short-Term Training.

PURPOSE: This study determined if the level of background physical inactivity (steps per day) influences the acute and short-term adaptations to intense aerobic training. METHODS: Sixteen untrained participants (23.6 ± 1.7 yr) completed intense (80%-90% V˙O2peak) short-term training (5 bouts of exercise over 9 d) while taking either 4767 ± 377 steps per day (n = 8; low step) or 16,048 ± 725 steps per day (n = 8; high step). At baseline and after 1 d of acute exercise and then after the short-term training (posttraining), resting metabolic responses to a high-fat meal (i.e., plasma triglyceride concentration and fat oxidation) were assessed during a 6-h high-fat tolerance test. In addition, responses during submaximal exercise were recorded both before and after training during 15 min of cycling (~79% of pretraining V˙O2peak). RESULTS: High step displayed a reduced incremental area under the curve for postprandial plasma triglyceride concentrations by 31% after acute exercise and by 27% after short-term training compared with baseline (P < 0.05). This was accompanied by increased whole-body fat oxidation (24% and 19%; P < 0.05). Furthermore, stress during submaximal exercise as reflected by heart rate, blood lactate, and deoxygenated hemoglobin were all reduced in high step (P < 0.05), indicating classic training responses. Despite completing the same training regimen, low step showed no significant improvements in postprandial fat metabolism or any markers of stress during submaximal exercise after training (P > 0.05). However, the two groups showed a similar 7% increase in V˙O2peak (P < 0.05). CONCLUSION: When completing an intense short-term exercise training program, decreasing daily background steps from 16,000 to approximately 5000 steps per day blunts some of the classic cardiometabolic adaptations to training. The blunting might be more pronounced regarding metabolic factors (i.e., fat oxidation and blood lactate concentration) compared with cardiovascular factors (i.e., V˙O2peak).

Four-Second Power Cycling Training Increases Maximal Anaerobic Power, Peak Oxygen Consumption, and Total Blood Volume.

INTRODUCTION: High-intensity interval training is an effective tool to improve cardiovascular fitness and maximal anaerobic power. Different methods of high-intensity interval training have been studied but the effects of repeated maximal effort cycling with very short exercise time (i.e., 4 s) and short recovery time (15-30 s) might suit individuals with limited time to exercise. PURPOSE: We examined the effects of training at near maximal anaerobic power during cycling (PC) on maximal anaerobic power, peak oxygen consumption (V˙O2peak), and total blood volume in 11 young healthy individuals (age: 21.3 ± 0.5 yr) (six men, five women). METHODS: Participants trained three times a week for 8 wk performing a PC program consisting of 30 bouts of 4 s at an all-out intensity (i.e., 2 min of exercise per session). The cardiovascular stress progressively increased over the weeks by decreasing the recovery time between sprints (30-24 s to 15 s), and thus, total session time decreased from 17 to <10 min. RESULTS: Power cycling elicited a 13.2% increase in V˙O2peak (Pre: 2.86 ± 0.18 L·min-1, Post: 3.24 ± 0.21 L·min-1; P = 0.003) and a 7.6% increase in total blood volume (Pre: 5139 ± 199 mL, Post: 5529 ± 342 mL; P < 0.05). Concurrently, maximal anaerobic power increased by 17.2% (Pre: 860 ± 53 W, Post: 1,009 ± 71 W; P < 0.001). CONCLUSIONS: A PC training program employing 30 bouts of 4 s duration for a total of 2 min of exercise, resulting in a total session time of less than 10 min in the last weeks, is effective for improving total blood volume, V˙O2peak and maximal anaerobic power in young healthy individuals over 8 wk. These observations require reconsideration of the minimal amount of exercise needed to significantly increase both maximal aerobic and anaerobic power.

Physiological responses to maximal 4 s sprint interval cycling using inertial loading: the influence of inter-sprint recovery duration.

PURPOSE: Interval exercise allows very high-power outputs to be maintained, a key for stimulating training adaptations. The main purpose of this study was to develop a sprint interval protocol that stimulated both anaerobic and aerobic systems while maximizing power output and minimizing fatigue. The secondary goal was to investigate the influence of inter-sprint recovery duration. METHODS: Sixteen (8 females) participants (age: 23.5 ± 3.4 years, peak oxygen consumption (VO2peak): 45.6 ± 9.2 ml kg-1 min-1) took part in this study. The exercise protocol involved 30 bouts of 4 s maximal cycling sprints using an 'Inertial Load Ergometer'. Recovery durations between sprints of 15, 30 and 45 s were studied in three trials. RESULTS: Peak power output (PPO) was maintained while taking 45 and 30 s of recovery, although it was 9% higher (p < 0.05) during 45 vs. 30 s. PPO with 15 s recovery declined 18% (p < 0.05) and then stabilized as did oxygen consumption (72±2% VO2peak) at a level that might reflect the peak rate of ATP-PC resynthesis from oxidative metabolism. The 15-, 30-, and 45 s trials elicited 72, 56, and 49% VO2peak and 86, 80, and 75% of maximal heart rate (all p<0.001). Perceived exertion increased with shorter recovery periods but remained at 12.6-14.7 and never became 'very hard'. CONCLUSION: The present study describes the use of an inertial-load ergometer to accommodate repeated 4 s maximal cycling sprints that elicit 72% VO2peak when the recovery period is 15 s. However, a recovery duration of 15 s was insufficient for the maintenance of power generation. TRIAL REGISTRATION NUMBER AND DATE: NCT04448925, 26 Jun 2020; retrospectively registered to clinicaltrials.gov.

Inertial Load Power Cycling Training Increases Muscle Mass and Aerobic Power in Older Adults.

PURPOSE: Reductions in skeletal muscle mass, beginning after the third decade of life, reduce maximal neuromuscular power (Pmax). Maximal aerobic power generation is also reduced. The primary purpose of this study was to investigate the effectiveness of maximal power cycling (PC) training using an inertial load ergometer on skeletal muscle mass and cardiovascular function in untrained 50- to 68-yr-old participants. METHODS: The study used a pre- or postoutcome exercise intervention testing untrained 50- to 68-yr-old adults (n = 39, M = 15, mean ± SE = 58.5 ± 0.8, range = 50-68 yr). Over the course of 8 wk, participants performed 15 min of training 3 times per week. Each session involved repeated (15-30 times) 4-s sprints of PC. Measurements were thigh muscle volume, total body lean mass, Pmax, peak oxygen consumption, cardio-ankle vascular index, performance on functional tests of living (FTLChair and FTLRamp), and intermuscular fat volume. RESULTS: Training for 8 wk increased thigh muscle volume (3.7% ± 0.9%, P < 0.001) and total body lean mass (1.5% ± 0.4%, P < 0.01) while increasing total body mass (TBM) (1.4% ± 0.3%, P < 0.01). Physical performance measures increased significantly (all P < 0.05) with improvements in Pmax (12.0% ± 1.5%); peak oxygen consumption (9.8% ± 1.8%), and FTL (8.5% ± 1.3% to 17.2% ± 2%). Cardio-ankle vascular index was significantly decreased -2.3% ± 1.1% (P < 0.05), indicating reduced arterial stiffness. CONCLUSIONS: These results demonstrate that 8 wk of PC training at true maximal power was effective at increasing muscle mass and maximal power, as well as maximal cardiovascular capacity and functional tasks in untrained 50- to 68-yr-olds.

Differences in joint power distribution in high and low lactate threshold cyclists.

PURPOSE: The biomechanical differences between cyclists with a high compared with a low blood lactate threshold (HLT; 80% VO2max vs LLT, 70% VO2max) have yet to be completely described. We hypothesize that HLT cyclists reduce the stress placed on the knee extensor muscles by increasing the relative contribution from the hip joint during high-intensity cycling. METHOD: Sixteen well-trained endurance athletes, with equally high VO2max while cycling and running completed submaximal tests during incremental exercise to identify lactate threshold ([Formula: see text]) while running and cycling. Subjects were separated into two groups based on % VO2max at LT during cycling (high; HLT: 80.2 ± 2.1% VO2max; n = 8) and (LLT: 70.3 ± 2.9% VO2max; n = 8; p < 0.01). Absolute and relative joint specific powers were calculated from kinematic and pedal forces using inverse dynamics while cycling at intensities ranging from 60-90% VO2max for between group comparisons. RESULT: There was no difference between HLT and LLT in [Formula: see text] (p > 0.05) while running. While cycling in LLT, knee joint absolute power increased with work rate (p < 0.05); however, in HLT no changes in knee joint absolute power occurred with increased work rate (p > 0.05). The HLT generated significantly greater relative hip power compared with the LLT group at 90% VO2max (p < 0.05). CONCLUSION: These data suggest that HLT cyclists exhibit a greater relative hip contribution to power output during cycling at 90% VO2max. These observations support the theory that lactate production during cycling can be reduced by spreading the work rate between various muscle groups.

Daily Step Count and Postprandial Fat Metabolism.

INTRODUCTION: Two benefits of acute exercise are the next day's lowering of the postprandial plasma triglyceride response to a high-fat meal and increased fat oxidation. However, if activity levels (daily steps) are very low, these acute adaptations to exercise do not occur. This phenomenon has been termed "exercise resistance." This study sought to systematically reduce daily step number and identify the range of step counts that elicit "exercise resistance." METHODS: Ten participants completed three, 5-d trials in a randomized, crossover design with differing levels of step reduction. After 2 d of controlled activity, participants completed 2 d of LOW, LIMITED, or NORMAL steps (2675 ± 314, 4759 ± 276, and 8481 ± 581 steps per day, respectively). Participants completed a 1-h bout of running on the evening of the second day. High-fat tolerance tests were performed on the next morning, and postprandial responses were compared. RESULTS: After LOW and LIMITED, postprandial incremental area under the curve (AUC) of plasma triglyceride was elevated 22%-23% compared with NORMAL (P < 0.05). Whole body fat oxidation was also significantly lower (16%-19%, P < 0.05, respectively) in LOW and LIMITED compared with NORMAL. No significant differences were found between LOW and LIMITED. CONCLUSION: Two days of step reduction to approximately 2500-5000 steps per day in young healthy individuals impairs the ability of an acute bout of exercise to increase fat oxidation and attenuate postprandial increases in plasma triglycerides. This suggests that "exercise resistance" occurs in individuals taking approximately 5000 or fewer steps per day, whereas 8500 steps per day protects against exercise resistance in fat metabolism. It seems that fat metabolism is influenced more by the inhibitory effects of inactivity than by the stimulating effects derived from 1 h of moderate-intensity running.

Hourly 4-s Sprints Prevent Impairment of Postprandial Fat Metabolism from Inactivity.

High postprandial plasma lipids (PPL; i.e., triglycerides) are a risk factor for cardiovascular disease. Physical inactivity, characterized by prolonged sitting and a low step count, elevates PPL and thus risk of disease. PURPOSE: This study determined if the interruption of prolonged sitting (i.e., 8 h of inactivity) with hourly cycling sprints of only 4-s duration each (i.e., 4 s × 5 per hour × 8 h = 160 s·d SPRINTS) improves PPL. The 4-s sprints used an inertial load ergometer and were followed by 45 s of seated rest. METHODS: Four men and four women participated in two trials. Interventions consisted of an 8-h period of sitting (SIT), or a trial with equal sitting time interrupted with five SPRINTS every hour. The morning after the interventions, PPL and fat oxidation were measured over a 6-h period. Plasma glucose, insulin, and triglyceride concentrations were measured bihourly and incremental area under the curve (AUC) was calculated. RESULTS: No differences (P > 0.05) between interventions were found for plasma insulin or glucose AUC. However, SPRINTS displayed a 31% (408 ± 119 vs 593 ± 88 mg·dL per 6 h; P = 0.009) decrease in plasma triglyceride incremental AUC and a 43% increase in whole-body fat oxidation (P = 0.001) when compared with SIT. CONCLUSIONS: These data indicate that hourly very short bouts (4 s) of maximal intensity cycle sprints interrupting prolonged sitting can significantly lower the next day's postprandial plasma triglyceride response and increase fat oxidation after a high-fat meal in healthy young adults. Given that these improvements were elicited from only 160 s of nonfatiguing exercise per day, it raises the question as to what is the least amount of exercise that can acutely improve fat metabolism and other aspects of health.

Prolonged standing reduces fasting plasma triglyceride but does not influence postprandial metabolism compared to prolonged sitting.

Prolonged periods of sedentary behavior are linked to cardiometabolic disease independent of exercise and physical activity. This study examined the effects of posture by comparing one day of sitting (14.4 ± 0.3 h) to one day of standing (12.2 ± 0.1 h) on postprandial metabolism the following day. Eighteen subjects (9 men, 9 women; 24 ± 1 y) completed two trials (sit or stand) in a crossover design. The day after prolonged sitting or standing the subjects completed a postprandial high fat/glucose tolerance test, during which blood and expired gas was collected immediately before and hourly for 6 h after the ingestion of the test meal. Indirect calorimetry was used to measure substrate oxidation while plasma samples were analyzed for triglyceride, glucose, and insulin concentrations. Standing resulted in a lower fasting plasma triglyceride concentration (p = 0.021) which was primarily responsible for an 11.3% reduction in total area under the curve (p = 0.022) compared to sitting. However, no difference between trials in incremental area under the curve for plasma triglycerides was detected (p>0.05). There were no differences in substrate oxidation, plasma glucose concentration, or plasma insulin concentration (all p>0.05). These data demonstrate that 12 h of standing compared to 14 h of sitting has a small effect the next day by lowering fasting plasma triglyceride concentration, and this contributed to a 11.3% reduction in postprandial plasma triglyceride total area under the curve (p = 0.022) compared to sitting.

Low Stroke Volume during Exercise with Hot Skin Is Due to Elevated Heart Rate.

It is well known that hyperthermia lowers stroke volume (SV) during moderate-intensity prolonged exercise, yet the underlying mechanism is inconclusive, especially when skin temperature (Tsk) is hot (≥38°C). PURPOSE: In the present study, HR was independently lowered by a low dose of ß1-blockade (ßB) to investigate its effect on SV during exercise when skin is hot. The effect of rapid skin cooling on reversing cardiovascular responses was also examined. METHODS: Nine men cycled at 62% V˙O2peak wearing a water-perfused suit for 20 min during three conditions: (a) moderate Tsk (~33°C) (MOD), (b) hot Tsk (~38°C) (HOT), and (c) hot Tsk (38°C) with ßB (HOT-ßB). Skin temperature was then rapidly cooled at 20 min in all trials by cold water (0°C-2°C) perfusion while subjects continued cycling for another 20 min. RESULTS: When HR was lowered during HOT-ßB (152 ± 4 bpm) to the same level as MOD (150 ± 4 bpm; P = 0.30), SV in HOT-ßB (132 ± 8 mL) was also restored to the same level as MOD (129 ± 7 mL, P = 0.37) even with a significantly higher cutaneous blood flow (CBF) and lower mean arterial blood pressure. When Tsk was rapidly cooled, cardiac output, HR, and CBF significantly decreased while SV remained lower in HOT. Forearm venous volume was not different between trials during heating and cooling. CONCLUSIONS: The increase in HR rather than an increase in CBF or forearm venous volume was responsible for the decrease in SV during moderate-intensity exercise when Tsk was held at 38°C.

Inactivity induces resistance to the metabolic benefits following acute exercise.

Acute exercise improves postprandial lipemia, glucose tolerance, and insulin sensitivity, all of which are risk factors for cardiovascular disease. However, recent research suggests that prolonged sedentary behavior might abolish these healthy metabolic benefits. Accordingly, this study aimed to elucidate the impact of an acute bout of exercise on postprandial plasma triglyceride, glucose, and insulin concentrations after 4 days of prolonged sitting (~13.5 h/day). Ten untrained to recreationally active men (n = 5) and women (n = 5) completed a counterbalanced, crossover study. Four days of prolonged sitting without exercise (SIT) were compared with 4 days of prolonged sitting with a 1-h bout of treadmill exercise (SIT + EX; 63.1 ± 5.2% V̇o2max) on the evening of the fourth day. The following morning, participants completed a high-fat/glucose tolerance test (HFGTT), during which plasma was collected over a 6-h period and analyzed for triglycerides, glucose, and insulin. No differences between trials (P > 0.05) were found in the overall plasma triglyceride, glucose, or insulin responses during the HFGTT. This lack of difference between trials comes with similarly low physical activity (~3,500-4,000 steps/day) on each day except for the 1-h bout of exercise during SIT + EX the day before the HFGTT. These data indicate that physical inactivity (e.g., sitting ~13.5 h/day and <4,000 steps/day) creates a condition whereby people become "resistant" to the metabolic improvements that are typically derived from an acute bout of aerobic exercise (i.e., exercise resistance). NEW & NOTEWORTHY In people who are physically inactive and sitting for a majority of the day, a 1-h bout of vigorous exercise failed to improve lipid, glucose, and insulin metabolism measured the next day. It seems that something inherent to inactivity and/or prolonged sitting makes the body resistant to the 1 h of exercise preventing the normally derived metabolic improvements following exercise.

The historical context and scientific legacy of John O. Holloszy.

John O. Holloszy, as perhaps the world's preeminent exercise biochemist/physiologist, published >400 papers over his 50+ year career, and they have been cited >41,000 times. In 1965 Holloszy showed for the first time that exercise training in rodents resulted in a doubling of skeletal muscle mitochondria, ushering in a very active era of skeletal muscle plasticity research. He subsequently went on to describe the consequences of and the mechanisms underlying these adaptations. Holloszy was first to show that muscle contractions increase muscle glucose transport independent of insulin, and he studied the mechanisms underlying this response throughout his career. He published important papers assessing the impact of training on glucose and insulin metabolism in healthy and diseased humans. Holloszy was at the forefront of rodent studies of caloric restriction and longevity in the 1980s, following these studies with important cross-sectional and longitudinal caloric restriction studies in humans. Holloszy was influential in the discipline of cardiovascular physiology, showing that older healthy and diseased populations could still elicit beneficial cardiovascular adaptations with exercise training. Holloszy and his group made important contributions to exercise physiology on the effects of training on numerous metabolic, hormonal, and cardiovascular adaptations. Holloszy's outstanding productivity was made possible by his mentoring of ~100 postdoctoral fellows and substantial NIH grant funding over his entire career. Many of these fellows have also played critical roles in the exercise physiology/biochemistry discipline. Thus it is clear that exercise biochemistry and physiology will be influenced by John Holloszy for numerous years to come.

Cardiovascular responses to exercise when increasing skin temperature with narrowing of the core-to-skin temperature gradient.

The decline in stroke volume (SV) during exercise in the heat has been attributed to either an increase in cutaneous blood flow (CBF) that reduces venous return or an increase in heart rate (HR) that reduces cardiac filling time. However, the evidence supporting each mechanism arises under experimental conditions with different skin temperatures (Tsk; e.g., ≥38°C vs. ≤36°C, respectively). We systematically studied cardiovascular responses to progressively increased Tsk (32°C-39°C) with narrowing of the core-to-skin gradient during moderate intensity exercise. Eight men cycled at 63 ± 1% peak oxygen consumption for 20-30 min. Tsk was manipulated by having subjects wear a water-perfused suit that covered most of the body and maintained Tsk that was significantly different between trials and averaged 32.4 ± 0.2, 35.5 ± 0.1, 37.5 ± 0.1, and 39.5 ± 0.1°C, respectively. The graded heating of Tsk ultimately produced a graded elevation of esophageal temperature (Tes) at the end of exercise. Incrementally increasing Tsk resulted in a graded increase in HR and a graded decrease in SV. CBF reached a similar average plateau value in all trials when Tes was above ~38°C, independent of Tsk. Tsk had no apparent effect on forearm venous volume (FVV). In conclusion, the CBF and FVV responses suggest no further pooling of blood in the skin when Tsk is increased from 32.4°C to 39.5°C. The decrease in SV during moderate intensity exercise when heating the skin to high levels appears related to an increase in HR and not an increase in CBF. NEW & NOTEWORTHY This study systematically investigated the effect of increasing skin temperature (Tsk) to high levels on cardiovascular responses during moderate intensity exercise. We conclude that the declines in stroke volume were related to the increases in heart rate but not the changes in cutaneous blood flow (CBF) and forearm venous volume (FVV) during moderate intensity exercise when Tsk increased from ~32°C to ~39°C. High Tsk (≥38°C) did not further elevate CBF and FVV compared with lower Tsk during moderate intensity exercise.

Prolonged sitting negatively affects the postprandial plasma triglyceride-lowering effect of acute exercise.

The interaction of prolonged sitting with physical exercise for maintaining health is unclear. We tested the hypothesis that prolonged siting would have a deleterious effect on postprandial plasma lipemia (PPL, postprandial plasma triglycerides) and reduce the ability of an acute exercise bout to attenuate PPL. Seven healthy young men performed three, 5-day interventions [days 1-5 (D1-D5)] in a randomized crossover design with >1 wk between interventions: 1) sitting > 14 h/day with hypercaloric energy balance (SH), 2) sitting >14 h/day with net energy balance (SB), and 3) active walking/standing with net energy balance (WB) and sitting 8.4 h/day. The first high-fat tolerance test (HFTT1) was performed on D3 following 2 days of respective interventions. On the evening of D4 subjects ran on a treadmill for 1 h at ~67% V̇o2max, followed by the second HFTT (HFTT2) on D5. Two days of prolonged sitting increased TG AUCI (i.e., incremental area under the curve for TG), irrespective of energy balance, compared with WB (27% in SH, P = 0.003 and 26% in SB, P = 0.046). Surprisingly, after 4 days of prolonged sitting (i.e.; SH and SB), the acute exercise on D4 failed to attenuate TG AUCI or increase relative fat oxidation in HFTT2, compared with HFTT1, regardless of energy balance. In conclusion, prolonged sitting over 2-4 days was sufficient to amplify PPL, which was not attenuated by acute exercise, regardless of energy balance. This underscores the importance of limiting sitting time even in people who have exercised.

Warm skin alters cardiovascular responses to cycling after preheating and precooling.

PURPOSE: Exercise in hot conditions increases core (TC) and skin temperature (TSK) and can lead to a progressive rise in HR and decline in stroke volume (SV) during prolonged exercise. Thermoregulatory-driven elevations in skin blood flow (SkBF) adds complexity to cardiovascular regulation during exercise in these conditions. Presently, the dominant, although debated, view is that raising TSK increases SkBF and reduces SV through diminished venous return; however, this scenario has not been rigorously investigated across core and skin temperatures. We tested the hypothesis that high TSK would raise HR and reduce SV during exercise after precooling (cold water bath) and preheating (hot water bath) and that no relationship would exist between SkBF and SV during exercise. METHODS: Non-endurance-trained individuals cycled for 20 min at 69% ± 1% VO2peak on four occasions: cool skin-cool core (SkCCC), warm skin-cool core (SkWCC), cool skin-warm core (SkCCW), and warm skin-warm core (SkWCW) on separate days. RESULTS: After precooling of TC, the rise in HR was greater in SkWCC than in SkCCC (P < 0.001), yet SV was similar (P = 0.26), which resulted in higher QC at min 20 in SkWCC (P < 0.01). Throughout exercise after preheating of TC, HR was higher (P < 0.001), SV was reduced (P < 0.01), and QC was similar (P = 0.40) in SkWCW versus SkCCW. When all trials were compared, there was no relationship between SkBF and SV (r = -0.08, P = 0.70); however, there was an inverse relationship between HR and SV (r = -0.75, P < 0.001). CONCLUSIONS: These data suggest that when TSK is elevated during exercise, HR and TC will rise but SV will only be reduced when TC is also elevated above 38°C. Furthermore, changes in SV are not related to changes in SkBF.