James P. Morton

High-intensity interval running is perceived to be more enjoyable than moderate-intensity continuous exercise: Implications for exercise adherence

Abstract The aim of this study was to objectively quantify ratings of perceived enjoyment using the Physical Activity Enjoyment Scale following high-intensity interval running versus moderate-intensity continuous running. Eight recreationally active men performed two running protocols consisting of high-intensity interval running (6×3 min at 90% [Vdot]O2max interspersed with 6×3 min active recovery at 50% [Vdot]O2max with a 7-min warm-up and cool down at 70% [Vdot]O2max) or 50 min moderate-intensity continuous running at 70% [Vdot]O2max. Ratings of perceived enjoyment after exercise were higher (P < 0.05) following interval running compared with continuous running (88 ± 6 vs. 61 ± 12) despite higher (P < 0.05) ratings of perceived exertion (14 ± 1 vs. 13 ± 1). There was no difference (P < 0.05) in average heart rate (88 ± 3 vs. 87 ± 3% maximum heart rate), average [Vdot]O2 (71 ± 6 vs. 73 ± 4%[Vdot]O2max), total [Vdot]O2 (162 ± 16 vs. 166 ± 27 L) or energy expenditure (811 ± 83 vs. 832 ± 136 kcal) between protocols. The greater enjoyment associated with high-intensity interval running may be relevant for improving exercise adherence, since running is a low-cost exercise intervention requiring no exercise equipment and similar relative exercise intensities have previously induced health benefits in patient populations.

The exercise-induced stress response of skeletal muscle, with specific emphasis on humans.

Skeletal muscle adapts to the stress of contractile activity via changes in gene expression to yield an increased content of a family of highly conserved cytoprotective proteins known as heat shock proteins (HSPs). These proteins function to maintain homeostasis, facilitate repair from injury and provide protection against future insults. The study of the exercise-induced production of HSPs in skeletal muscle is important for the exercise scientist as it may provide a valuable insight into the molecular mechanisms by which regular exercise can provide increased protection against related and non-related stressors. As molecular chaperones, HSPs are also fundamental in facilitating the cellular remodelling processes inherent to the training response.Whilst the exercise-induced stress response of rodent skeletal muscle is relatively well characterized, data from humans are more infrequent and less insightful. Data indicate that acute endurance- and resistance-type exercise protocols increase the muscle content of ubiquitin, aB-crystallin, HSP27, HSP60, HSC70 and HSP70. Although increased HSP transcription occurs during exercise, immediately post-exercise or several hours following exercise, time-course studies using western blotting techniques have typically demonstrated a significant increase in protein content is only detectable within 1–2 days following the exercise stress. However, comparison amongst studies is complicated by variations in exercise protocol (mode, intensity, duration, damaging, non-damaging), muscle group examined, predominant HSP measured and, perhaps most importantly, differences in subject characteristics both within and between studies (training status, recent activity levels, nutritional status, age, sex, etc.). Following ‘non-damaging’ endurancetype activities (exercise that induces no overt structural and functional damage to the muscle), the stress response is thought to be mediated by redox signalling (transient and reversible oxidation of muscle proteins) as opposed to increases in contracting muscle temperature per se. Following ‘damaging’ forms of exercise (exercise that induces overt structural and functional damage to the muscle), the stress response is likely initiated by mechanical damage to protein structure and further augmented by the secondary damage associated with inflammatory processes occurring several days following the initial insult. Exercise training induces an increase in baseline HSP levels, which is dependent on a sustained and currently unknown dose of training and also on the individual’s initial training status. Furthermore, trained subjects display an attenuated or abolished stress response to customary exercise challenges, likely due to adaptations of baseline HSP levels and the antioxidant system.Whilst further fundamental work is needed to accurately characterize the exercise-induced stress response in specific populations following varying exercise protocols, exercise scientists should also focus their efforts on elucidating the precise biological significance of the exercise-induced induction of HSPs. In addition to their potential cytoprotective properties, the role of HSPs in modulating cell signalling pathways related to both exercise adaptation and health and disease also needs further investigation. As a nonpharmacological intervention, exercise and the associated up-regulation of HSPs and the possible correction of maladapted pathways may therefore prove effective in providing protection against protein misfolding diseases and in preserving muscle function during aging.

Reduced carbohydrate availability does not modulate training-induced heat shock protein adaptations but does upregulate oxidative enzyme activity in human skeletal muscle

The primary aim of the present study was to test the hypothesis that training with reduced carbohydrate availability from both endogenous and exogenous sources provides an enhanced stimulus for training-induced heat shock protein (HSP) adaptations of skeletal muscle. A secondary aim was to investigate the influence of reduced carbohydrate availability on oxidative adaptations and exercise performance. Three groups of recreationally active men performed 6 wk of high-intensity intermittent running occurring four times per week. Group 1 (n = 8; Low + Glu) and 2 (n = 7; Low + Pla) trained twice per day, 2 days/wk, and consumed a 6.4% glucose or placebo solution, respectively, immediately before every second training session and at regular intervals throughout exercise. Group 3 (n = 8; Norm) trained once per day, 4 days/wk, and consumed no beverage throughout training. Training induced significant improvements in maximal oxygen uptake (Vo(2max)) (P = 0.001) and distance covered on Yo-Yo Intermittent Recovery Test 2 (P = 0.001) in all groups, with no difference between conditions. Similarly, training resulted in significant increases in HSP70, HSP60, and alphaB-crystallin in the gastrocnemius (P = 0.03, 0.02, and 0.01, respectively) and vastus lateralis (P = 0.01, 0.02, and 0.003, respectively) muscles in all groups, with no difference between conditions. In contrast, training resulted in significant increases in succinate dehydrogenase (SDH) activity of the gastrocnemeius (Low + Glu, Low + Pla, and Norm: 27, 76, and 53% increases, respectively; P = 0.001) and vastus lateralis muscles (Low + Glu, Low + Pla, and Norm: 17, 70, and 19% increases, respectively; P = 0.001) where the magnitude of increase in SDH activity was significantly larger for both muscles (P = 0.03 and 0.04 for gastrocnemius and vastus lateralis, respectively) for subjects training in the Low + Pla condition. Data provide the first evidence that in whole body exercise conditions, carbohydrate availability appears to have no modulating effect on training-induced increases of the HSP content of skeletal muscle. In contrast, training under conditions of reduced carbohydrate availability from both endogenous and exogenous sources provides an enhanced stimulus for inducing oxidative enzyme adaptations of skeletal muscle although this does not translate to improved performance during high-intensity exercise.

Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle

The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 × 3-min at 90% maximal oxygen consumption (Vo(2max)) interspersed with 3-min recovery periods at 50% Vo(2max) with a 7-min warm-up and cool-down period at 70% Vo(2max)] or CONT (50-min continuous running at 70% Vo(2max)). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 ± 11 vs. 111 ± 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 ± 0.1- vs. 1.5 ± 0.2-fold) and AMPK(Thr172) (1.5 ± 0.3- vs. 1.5 ± 0.1-fold) increased immediately postexercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53(Ser15) (HIT, 2.7 ± 0.8-fold; CONT, 2.1 ± 0.8-fold), PGC-1α mRNA (HIT, 4.2 ± 1.7-fold; CONT, 4.5 ± 0.9-fold) and HSP72 mRNA (HIT, 4.4 ± 2-fold; CONT, 3.5 ± 1-fold) all increased 3 h postexercise (P < 0.05) although neither parameter increased (P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses (P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.

Assessment of vitamin D concentration in non-supplemented professional athletes and healthy adults during the winter months in the UK: implications for skeletal muscle function

Abstract The current study implemented a two-part design to (1) assess the vitamin D concentration of a large cohort of non-vitamin D supplemented UK-based athletes and 30 age-matched healthy non-athletes and (2) to examine the effects of 5000 IU · day−1 vitamin D3 supplementation for 8-weeks on musculoskeletal performance in a placebo controlled trial. Vitamin D concentration was determined as severely deficient if serum 25(OH)D < 12.5 nmol · l−1, deficient 12.5–30 nmol · l−1 and inadequate 30–50 nmol · l−1. We demonstrate that 62% of the athletes (38/61) and 73% of the controls (22/30) exhibited serum total 25(OH)D < 50 nmol · l−1. Additionally, vitamin D supplementation increased serum total 25(OH)D from baseline (mean ± SD = 29 ± 25 to 103 ± 25 nmol · l−1, P = 0.0028), whereas the placebo showed no significant change (53 ± 29 to 74 ± 24 nmol · l−1, P = 0.12). There was a significant increase in 10 m sprint times (P = 0.008) and vertical-jump (P = 0.008) in the vitamin D group whereas the placebo showed no change (P = 0.587 and P = 0.204 respectively). The current data supports previous findings that athletes living at Northerly latitudes (UK = 53° N) exhibit inadequate vitamin D concentrations (<50 nmol · l−1). Additionally the data suggests that inadequate vitamin D concentration is detrimental to musculoskeletal performance in athletes. Future studies using larger athletic groups are now warranted.

Influence of Cold Water Immersion on Limb and Cutaneous Blood Flow at Rest

Background: Cold water immersion reduces exercise-induced muscle damage. Benefits may partly arise from a decline in limb blood flow; however, no study has comprehensively investigated the influence of different degrees of cooling undertaken via cold water immersion on limb blood flow responses. Purpose: To determine the influence of cold (8°C) and cool (22°C) water immersion on lower limb and cutaneous blood flow. Study Design: Controlled laboratory study. Methods: Nine men were placed in a semireclined position and lowered into 8°C or 22°C water to the iliac crest for two 5-minute periods interspersed with 2 minutes of nonimmersion. Rectal and thigh skin temperature, deep and superficial muscle temperature, heart rate, mean arterial pressure, thigh cutaneous blood velocity (laser Doppler), and superficial femoral artery blood flow (duplex ultrasound) were measured during immersion and for 30 minutes after immersion. Indices of vascular conductance were calculated (flux and blood flow/mean arterial pressure). Results: Reductions in rectal temperature (8°C, 0.2° ± 0.1°C; 22°C, 0.1° ± 0.1°C) and thigh skin temperature (8°C, 6.2° ± 0.5°C; 22°C, 3.2° ± 0.2°C) were greater in 8°C water than in 22°C (P < .01). Femoral artery conductance was reduced to a similar extent immediately after immersion (~30%) and 30 minutes after immersion (~40%) under both conditions (P < .01). In contrast, there was less thigh cutaneous vasoconstriction during and after immersion in 8°C water compared with 22°C (P = .01). Conclusion: These data suggest that immersion at both temperatures resulted in similar whole limb blood flow but, paradoxically, more blood was distributed to the skin in the colder water. This suggests that colder temperatures may be associated with reduced muscle blood flow, which could provide an explanation for the benefits of cold water immersion in alleviating exercise-induced muscle damage in sports and athletic contexts. Clinical Relevance: Colder water temperatures may be more effective in the treatment of exercise-induced muscle damage and injury rehabilitation because of greater reductions in muscle blood flow.

Carbohydrate availability and exercise training adaptation: Too much of a good thing?

Abstract Traditional nutritional approaches to endurance training have typically promoted high carbohydrate (CHO) availability before, during and after training sessions to ensure adequate muscle substrate to meet the demands of high daily training intensities and volumes. However, during the past decade, data from our laboratories and others have demonstrated that deliberately training in conditions of reduced CHO availability can promote training-induced adaptations of human skeletal muscle (i.e. increased maximal mitochondrial enzyme activities and/or mitochondrial content, increased rates of lipid oxidation and, in some instances, improved exercise capacity). Such data have led to the concept of ‘training low, but competing high’ whereby selected training sessions are completed in conditions of reduced CHO availability (so as to promote training adaptation), but CHO reserves are restored immediately prior to an important competition. The augmented training response observed with training-low strategies is likely regulated by enhanced activation of key cell signalling kinases (e.g. AMPK, p38MAPK), transcription factors (e.g. p53, PPARδ) and transcriptional co-activators (e.g. PGC-1α), such that a co-ordinated up-regulation of both the nuclear and mitochondrial genomes occurs. Although the optimal practical strategies to train low are not currently known, consuming additional caffeine, protein, and practising CHO mouth-rinsing before and/or during training may help to rescue the reduced training intensities that typically occur when ‘training low’, in addition to preventing protein breakdown and maintaining optimal immune function. Finally, athletes should practise ‘train-low’ workouts in conjunction with sessions undertaken with normal or high CHO availability so that their capacity to oxidise CHO is not blunted on race day.

Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: Implications for mitochondrial biogenesis

The mechanisms that regulate the enhanced skeletal muscle oxidative capacity observed when training with reduced carbohydrate (CHO) availability are currently unknown. The aim of the present study was to test the hypothesis that reduced CHO availability enhances p53 signaling and expression of genes associated with regulation of mitochondrial biogenesis and substrate utilization in human skeletal muscle. In a repeated-measures design, muscle biopsies (vastus lateralis) were obtained from eight active males before and after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). Resting muscle glycogen (HIGH, 467 ± 19; LOW, 103 ± 9 mmol/kg dry wt) was greater in HIGH compared with LOW (P < 0.05). Phosphorylation (P-) of ACC(Ser79) (HIGH, 1.4 ± 0.4; LOW, 2.9 ± 0.9) and p53(Ser15) (HIGH, 0.9 ± 0.4; LOW, 2.6 ± 0.8) was higher in LOW immediately postexercise and 3 h postexercise, respectively (P < 0.05). Before and 3 h postexercise, mRNA content of pyruvate dehydrogenase kinase 4, mitochondrial transcription factor A, cytochrome-c oxidase IV, and PGC-1α were greater in LOW compared with HIGH (P < 0.05), whereas carnitine palmitoyltransferase-1 showed a trend toward significance (P = 0.09). However, only PGC-1α expression was increased by exercise (P < 0.05), where three-fold increases occurred independently of CHO availability. We conclude that the exercise-induced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK. Given the emergence of p53 as a molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation has implications for both athletic and clinical populations.

Proteomic investigation of changes in human vastus lateralis muscle in response to interval-exercise training.

No previous study has used proteomics to investigate the effects of exercise training on human skeletal muscle. Five recreationally active men completed a 6‐wk training programme involving three sessions per week, utilising six 1‐min bouts at maximum oxygen uptake (V̇ O2max) interspersed with 4 min at 50% V̇ O2max. Vastus lateralis was biopsied at standardised times before and after the training intervention. Protein expression profiling was performed using differential analysis of 2‐DE gels; complemented with quantitative analysis (iTRAQ) of tryptic peptides from 1‐DE gel lane‐segments using LC‐MALDI MS/MS. Interval training increased average V̇ O2max (7%; p<0.001) and was associated with greater expression of mitochondrial components, including succinate dehydrogenase, trifunctional protein‐α and ATP synthase α‐ and β‐chains. 2‐DE resolved 256 spots, and paired t‐tests identified 20 significant differences in expression (false discovery rate <10%). Each differentially expressed gene product was present as multiple isoelectric species. Therefore, the differences in spot expression represent changes in post‐transcriptional or post‐translational processing. In particular, modulation of muscle creatine kinase and troponin T were prominent. Pro‐Q Diamond staining revealed these changes in expression were associated with phosphorylated protein species, which provides novel information regarding muscle adaptation to interval training.

The effects of vitamin D(3) supplementation on serum total 25[OH]D concentration and physical performance:a randomised dose-response study

Background Vitamin D deficiency is common in the general public and athletic populations and may impair skeletal muscle function. We therefore assessed the effects of vitamin D3 supplementation on serum 25[OH]D concentrations and physical performance. Methods 30 club-level athletes were block randomised (using baseline 25[OH]D concentrations) into one of three groups receiving either a placebo (PLB), 20 000 or 40 000 IU/week oral vitamin D3 for 12 weeks. Serum 25[OH]D and muscle function (1-RM bench press and leg press and vertical jump height) were measured presupplementation, 6 and 12 weeks postsupplementation. Vitamin D deficiency was defined in accordance with the US Institute of Medicine guideline (<50 nmol/l). Results 57% of the subject population were vitamin D deficient at baseline (mean±SD value 51±24 nmol/l). Following 6 and 12 weeks supplementation with 20 000 IU (79±14 and 85±10 nmol/l, respectively) or 40 000 IU vitamin D3 (98±14 and 91±24 nmol/l, respectively), serum vitamin D concentrations increased in all participants, with every individual achieving concentrations greater than 50 nmol/l. In contrast, vitamin D concentration in the PLB group decreased at 6 and 12 weeks (37±18 and 41±22 nmol/l, respectively). Increasing serum 25[OH]D had no significant effect on any physical performance parameter (p>0.05). Conclusions Both 20 000 and 40 000 IU vitamin D3 supplementation over a 6-week period elevates serum 25[OH]D concentrations above 50 nmol/l, but neither dose given for 12 weeks improved our chosen measures of physical performance.