It is typically assumed that in the context of double-leg cycling, dominant (DOM
) and nondominant legs (NDOM
) have similar aerobic capacity and both contribute equally to the whole body ...physiological responses. However, there is a paucity of studies that have systematically investigated maximal and submaximal aerobic performance and characterized the profiles of local muscle deoxygenation in relation to leg dominance. Using counterweighted single-leg cycling, this study explored whether peak O
consumption (V̇o
), maximal lactate steady-state (MLSS
), and profiles of local deoxygenation HHb would be different in the DOM
compared with the NDOM
. Twelve participants performed a series of double-leg and counterweighted single-leg DOM
and NDOM
ramp-exercise tests and 30-min constant-load trials. V̇o
was greater in the DOM
than in the NDOM
(2.87 ± 0.42 vs. 2.70 ± 0.39 L/min,
< 0.05). The difference in V̇o
persisted even after accounting for lean mass (
< 0.05). Similarly, MLSS
was greater in the DOM
than in the NDOM
(118 ± 31 vs. 109 ± 31 W;
< 0.05). Furthermore, the amplitude of the HHb signal during ramp exercise was larger in the DOM
than in the NDOM
during both double-leg (26.0 ± 8.4 vs. 20.2 ± 8.8 µM,
< 0.05) and counterweighted single-leg cycling (18.5 ± 7.9 vs. 14.9 ± 7.5 µM,
< 0.05). Additionally, the amplitudes of the HHb signal were highly to moderately correlated with the mode-specific V̇o
values (ranging from 0.91 to 0.54). These findings showed in a group of young men that maximal and submaximal aerobic capacities were greater in the DOM
than in the NDOM
and that superior peripheral adaptations of the DOM
may underpin these differences.
It is typically assumed that the dominant and nondominant legs contribute equally to the whole physiological responses. In this study, we found that the dominant leg achieved greater peak O
uptake values, sustained greater power output while preserving whole body metabolic stability, and showed larger amplitudes of deoxygenation responses. These findings highlight heterogeneous aerobic capacities of the lower limbs, which have important implications when whole body physiological responses are examined.
The legs of 9 men (age 21 ± 2 years, 45 ± 4 mL/(kg·min)) were randomly assigned to complete 6 sessions of high-intensity exercise training, involving either one or four 5-min bouts of ...counterweighted, single-leg cycling. Needle biopsies from vastus lateralis revealed that citrate synthase maximal activity increased after training in the 4-bout group (p = 0.035) but not the 1-bout group (p = 0.10), with a significant difference between groups post-training (13%, p = 0.021).
Novelty
Short-term training using brief intense exercise requires multiple bouts per session to increase mitochondrial content in human skeletal muscle.
The aims of the present study were to investigate blood lactate kinetics following high intensity exercise and identify the physiological determinants of 800 m running performance.
Fourteen ...competitive 800 m runners performed two running tests. First, participants performed a multistage graded exercise test to determine physiological indicators related to endurance performance. Second, participants performed four to six 30-s high intensity running bouts to determine post-exercise blood lactate kinetics. Using a biexponential time function, lactate exchange ability (γ
), lactate removal ability (γ
), and the quantity of lactate accumulated (QLaA) were calculated from individual blood lactate recovery data.
800 m running performance was significantly correlated with peak oxygen consumption (r = -0.794), γ
and γ
at 800 m race pace (r = -0.604 and -0.845, respectively), and QLaA at maximal running speed (r = -0.657).
O
and γ
at 800 m race pace explained 83% of the variance in 800 m running performance.
Our results indicate that (1) a high capacity to exchange and remove lactate, (2) a high capacity for short-term lactate accumulation and, (3) peak oxygen consumption, are critical elements of 800 m running performance. Accordingly, while lactate has primarily been utilized as a performance indicator for long-distance running, post-exercise lactate kinetics may also prove valuable as a performance determinant in middle-distance running.
New Findings
What is the central question of this study?
Are there sex‐based differences in the acute skeletal muscle response to sprint interval training (SIT)?
What is the main finding and its ...importance?
In response to a SIT protocol that involved three 20 s bouts of ‘all‐out’ cycling, the expression of multiple genes associated with mitochondrial biogenesis, metabolic control and structural remodelling was largely similar between men and women matched for fitness. Our findings cannot explain previous reports of sex‐based differences in the adaptive response to SIT and suggest that the mechanistic basis for these differences remains to be elucidated.
A few studies have reported sex‐based differences in response to several weeks of sprint interval training (SIT). These findings may relate to sex‐specific responses to an acute session of SIT. We tested the hypothesis that the acute skeletal muscle response to SIT differs between sexes. Sedentary but healthy men (n = 10) and women (n = 9) were matched for age (22 ± 3 versus 22 ± 3 years old) and cardiorespiratory fitness 45 ± 7 versus 43 ± 10 ml O2 (kg fat‐free mass)−1 min−1, with women tested in the mid‐follicular phase of their menstrual cycles. Subjects performed three 20 s ‘all‐out’ cycling efforts against a resistance of 5% of body mass, interspersed with 2 min of recovery. Relative mean power outputs 7.6 ± 0.5 versus 7.5 ± 0.9 W (kg fat‐free mass)−1 were similar between men and women (P > 0.05). Furthermore, there were no differences in the exercise‐induced changes in mRNA expression of PGC‐1α, PRC, PPARD, SIRT1, RIP140, HSL, HKII, PDK4, PDP1, FOXO3, MURF‐1, Myf5, MyoD and VEGFA at 3 h of recovery versus rest (P < 0.05, main effect of time). The only sex‐specific responses to exercise were an increase in the mRNA expression of GLUT4 and LPL in women only and Atrogin‐1 in men only (P < 0.05). Women also had higher expression of HKII and lower expression of FOXO3 compared with men (P < 0.05, main effect of sex). We conclude that the acute skeletal muscle response to SIT is largely similar in young men and women. The mechanistic basis for sex‐based differences in response to several weeks of SIT that has been previously reported remains to be elucidated.
Sprint interval training (SIT) causes fragmentation of the skeletal muscle sarcoplasmic reticulum Ca2+ release channel, ryanodine receptor 1 (RyR1), 24 h post‐exercise, potentially signalling ...mitochondrial biogenesis by increasing cytosolic Ca2+. Yet, the time course and skeletal muscle fibre type‐specific patterns of RyR1 fragmentation following a session of SIT remain unknown. Ten participants (n = 4 females; n = 6 males) performed a session of SIT (6 × 30 s ‘all‐out’ with 4.5 min rest after each sprint) with vastus lateralis muscle biopsy samples collected before and 3, 6 and 24 h after exercise. In whole muscle, full‐length RyR1 protein content was significantly reduced 6 h (mean (SD); −38 (38)%; P < 0.05) and 24 h post‐SIT (−30 (48)%; P < 0.05) compared to pre‐exercise. Examining each participant's largest response in pooled samples, full‐length RyR1 protein content was reduced in type II (−26 (30)%; P < 0.05) but not type I fibres (−11 (40)%; P > 0.05). Three hours post‐SIT, there was also a decrease in sarco(endo)plasmic reticulum Ca2+ ATPase 1 in type II fibres (−23 (17)%; P < 0.05) and sarco(endo)plasmic reticulum Ca2+ ATPase 2a in type I fibres (−19 (21)%; P < 0.05), despite no time effect for either protein in whole muscle samples (P > 0.05). PGC1A mRNA content was elevated 3 and 6 h post‐SIT (5.3‐ and 3.7‐fold change from pre, respectively; P < 0.05 for both), but peak PGC1A mRNA expression was not significantly correlated with peak RyR1 fragmentation (r2 = 0.10; P > 0.05). In summary, altered Ca2+‐handling protein expression, which occurs primarily in type II muscle fibres, may influence signals for mitochondrial biogenesis as early as 3–6 h post‐SIT in humans.
Key points
Sprint interval training (SIT) has been shown to cause fragmentation of the sarcoplasmic reticulum calcium‐release channel, ryanodine receptor 1 (RyR1), 24 h post‐exercise, which may act as a signal for mitochondrial biogenesis.
In this study, the time course was examined of RyR1 fragmentation in human whole muscle and pooled type I and type II skeletal muscle fibres following a single session of SIT.
Full‐length RyR1 protein content was significantly lower than pre‐exercise by 6 h post‐SIT in whole muscle, and fragmentation was detectable in type II but not type I fibres, though to a lesser extent than in whole muscle.
The peak in PGC1A mRNA expression occurred earlier than RyR1 fragmentation.
The increased temporal resolution and fibre type‐specific responses for RyR1 fragmentation provide insights into its importance to mitochondrial biogenesis in humans.
figure legend Western blotting was performed on whole muscle and pooled type I and II muscle fibre preparations derived from human vastus lateralis muscle biopsy samples collected before and after a single session of sprint interval training (SIT). Full‐length ryanodine receptor 1 (RyR1) protein content was reduced 6 and 24 h post‐exercise in whole muscle samples compared to baseline, despite a heterogeneous time course among individuals. This RyR1 fragmentation proceeded and outlasted the increase in peroxisome proliferator‐activated γ receptor coactivator 1α (PGC1A) mRNA expression. When examining the time point of each individual's peak response, RyR1 fragmentation was evident in type II, but not type I, muscle fibres. These findings suggest that, in humans, mitochondrial biogenesis could be influenced by RyR1 fragmentation 3–6 h post‐SIT in a fibre type‐dependent manner. Created with BioRender.com.
To further refine the near-infrared spectroscopy (NIRS)-derived measure of skeletal muscle oxidative capacity in humans, we sought to determine whether the exercise stimulus intensity affected the τ ...value and/or influenced the magnitude of correlations with in vitro measures of mitochondrial content and in vivo indices of exercise performance. Males (
= 12) and females (
= 12), matched for maximal aerobic fitness per fat-free mass, completed NIRS-derived skeletal muscle oxidative capacity tests for the vastus lateralis following repeated contractions at 40% (τ
) and 100% (τ
) of maximum voluntary contraction, underwent a skeletal muscle biopsy of the same muscle, and performed multiple intermittent isometric knee extension tests to task failure to establish critical torque (CT). The value of τ
(34.4 ± 7.0 s) was greater than τ
(24.2 ± 6.9 s,
< 0.001), but the values were correlated (
= 0.688;
< 0.001). The values of τ
(
= -0.692,
< 0.001) and τ
(
= -0.488,
= 0.016) correlated with myosin heavy chain I percentage and several markers of mitochondrial content, including COX II protein content in whole muscle (τ
:
= -0.547,
= 0.006; τ
:
= -0.466,
= 0.022), type I pooled fibers (τ
:
= -0.547,
= 0.006; τ
:
= -0.547,
= 0.006), and type II pooled fibers (τ
:
= -0.516,
= 0.009; τ
:
= -0.635,
= 0.001). The value of τ
(
= -0.702,
< 0.001), but not τ
(
= -0.378,
= 0.083) correlated with critical torque (CT); however, neither value correlated with W' (τ
:
= 0.071,
= 0.753; τ
:
= 0.054,
= 0.812). Overall, the NIRS method of assessing skeletal muscle oxidative capacity is sensitive to the intensity of skeletal muscle contraction but maintains relationships to whole body fitness, isolated limb critical intensity, and mitochondrial content regardless of intensity.
Skeletal muscle oxidative capacity measured using near-infrared spectroscopy (NIRS) was lower following high-intensity compared with low-intensity isometric knee extension contractions. At both intensities, skeletal muscle oxidative capacity was correlated with protein markers of mitochondrial content (in whole muscle and pooled type I and type II muscle fibers) and critical torque. These findings highlight the importance of standardizing contraction intensity while using the NIRS method with isometric contractions and further demonstrate its validity.
Green tea extract (GTE) ingestion improves glucose homeostasis in healthy and diabetic humans, but the interactive effect of GTE and exercise is unknown. The present study examined the effect of ...short-term GTE supplementation on the glycemic response to an oral glucose load at rest and following an acute bout of exercise, as well as substrate oxidation during exercise. Eleven sedentary, overweight men with fasting plasma glucose (FPG) ≥5.6 mmol·L
−1
(age, 34 ± 13 years; body mass index = 32 ± 5 kg·m
−2
; FPG = 6.8 ± 1.0; mean ± SD) ingested GTE (3× per day, 1050 mg·day
–1
total) or placebo (PLA) for 7 days in a double-blind, crossover design. The effects of a 75-g glucose drink were assessed on 4 occasions during both GTE and PLA treatments: On days 1 and 5 at rest, and again following an acute bout of exercise on days 3 and 8. The glycemic response was assessed via an indwelling continuous glucose monitor (CGM) and venous blood draws. At rest, 1-h CGM glucose area under the curve was not different (P > 0.05), but the postexercise response was lower after GTE versus PLA (330 ± 53 and 393 ± 65 mmol·L
−1
·min
−1
, main effect of treatment, P < 0.05). The 1-h postprandial peaks in venous blood glucose (8.6 ± 1.6 and 9.8 ± 2.2 mmol·L
−1
) and insulin (96 ± 59 and 124 ± 68 μIU·ml
−1
) were also lower postexercise with GTE versus PLA (time × treatment interactions, P < 0.05). In conclusion, short-term GTE supplementation did not affect postprandial glucose at rest; however, GTE was associated with an attenuated glycemic response following a postexercise oral glucose load. These data suggest that GTE might alter skeletal muscle glucose uptake in humans.
There is renewed interest in the potential for interval (INT) training to increase skeletal muscle mitochondrial content including whether the response differs from continuous (CONT) training. ...Comparisons of INT and CONT exercise are impacted by the manner in which protocols are “matched”, particularly with respect to exercise intensity, as well as inter‐individual differences in training responses. We employed single‐leg cycling to facilitate a within‐participant design and test the hypothesis that short‐term INT training would elicit a greater increase in mitochondrial content than work‐ and intensity‐matched CONT training. Ten young healthy adults (five males and five females) completed 12 training sessions over 4 weeks with each leg. Legs were randomly assigned to complete either 30 min of CONT exercise at a challenging sustainable workload (~50% single‐leg peak power output; Wpeak) or INT exercise that involved 10 × 3‐min bouts at the same absolute workload. INT bouts were interspersed with 1 min of recovery at 10% Wpeak and each CONT session ended with 10 min at 10% Wpeak. Absolute and mean intensity, total training time, and volume were thus matched between legs but the pattern of exercise differed. Contrary to our hypothesis, biomarkers of mitochondrial content including citrate synthase maximal activity, mitochondrial protein content and subsarcolemmal mitochondrial volume increased after CONT (p < 0.05) but not INT training. Both training modes increased single‐leg Wpeak (p < 0.01) and time to exhaustion at 70% of single‐leg Wpeak (p < 0.01). In a work‐ and intensity‐matched comparison, short‐term CONT training increased skeletal muscle mitochondrial content whereas INT training did not.
Critical torque (CT) represents the highest oxidative steady state for intermittent knee extensor exercise, but the extent to which it is influenced by skeletal muscle mitochondria and sex is ...unclear. Vastus lateralis muscle biopsy samples were collected from 12 females and 12 males –matched for relative maximal oxygen uptake normalized to fat‐free mass (FFM) (F: 57.3 (7.5) ml (kg FFM)−1 min−1; M: 56.8 (7.6) ml (kg FFM)−1 min−1; P = 0.856) – prior to CT determination and performance fatiguability trials. Males had a lower proportion of myosin heavy chain (MHC) I isoform (40.6 (18.4)%) compared to females (59.5 (18.9)%; P = 0.021), but MHC IIa and IIx isoform distributions and protein markers of mitochondrial content were not different between sexes (P > 0.05). When normalized to maximum voluntary contraction (MVC), the relative CT (F: 42.9 (8.3)%; M: 37.9 (9.0)%; P = 0.172) and curvature constant, W′ (F: 26.6 (11.0) N m s (N m)−1; M: 26.4 (6.5) N m s (N m)−1; P = 0.962) were not significantly different between sexes. All protein biomarkers of skeletal muscle mitochondrial content, as well as the proportion of MHC I isoform, positively correlated with relative CT (0.48 < r < 0.70; P < 0.05), and the proportion of MHC IIx isoform correlated positively with relative W′ (r = 0.57; P = 0.007). Indices of performance fatiguability were not different between males and females for MVC‐ and CT‐controlled trials (P > 0.05). Greater mitochondrial protein abundance was associated with attenuated declines in potentiated twitch torque for exercise at 60% MVC (P < 0.05); however, the influence of mitochondrial protein abundance on performance fatiguability was reduced when exercise was prescribed relative to CT. Whether these findings translate to whole‐body exercise requires additional research.
Key points
The quadriceps critical torque represents the highest intensity of intermittent knee extensor exercise for which an oxidative steady state is attainable, but its relationship with skeletal muscle mitochondrial protein abundance is unknown.
Matching males and females for maximal oxygen uptake relative to fat‐free mass facilitates investigations of sex differences in exercise physiology, but studies that have compared critical torque and performance fatiguability during intermittent knee extensor exercise have not ensured equal aerobic fitness between sexes.
Skeletal muscle mitochondrial protein abundance was correlated with critical torque and fatigue resistance for exercise prescribed relative to maximum voluntary contraction but not for exercise performed relative to the critical torque.
Differences between sexes in critical torque, skeletal muscle mitochondrial protein abundance and performance fatiguability were not statistically significant.
Our results suggest that skeletal muscle mitochondrial protein abundance may contribute to fatigue resistance by influencing the critical intensity of exercise.
figure legend Critical torque (CT), performance fatiguability, and skeletal muscle mitochondrial protein content and fibre type were determined for males (M) and females (F) matched for peak oxygen uptake (V̇O2peak${\dot{V}}_{{\mathrm{O}}_{2}\mathrm{peak}}$) per fat‐free mass. The CT and mitochondrial protein content were not significantly different between sexes. Mitochondrial protein content correlated with CT but not the curvature constant, W′. Mitochondrial protein content correlated with fatiguability when intermittent, isometric knee extensor exercise was performed to task failure at 60% MVC but not when it was performed for 30 min 10% below CT.
Many skeletal muscle proteins are present in a cell-specific or fibre-type dependent manner. Stimuli such as exercise, aging, and disease have been reported to result in fibre-specific responses in ...protein abundances. Thus, fibre-type-specific determination of the content of specific proteins provides enhanced mechanistic understanding of muscle physiology and biochemistry compared with typically performed whole-muscle homogenate analyses. This analysis, however, is laborious and typically not performed. We present a novel dot blotting method for easy and rapid determination of skeletal muscle fibre type based on myosin heavy chain (MHC) isoform presence. Requiring only small amounts of starting muscle tissue (i.e., 2-10 mg wet weight), muscle fibre type is determined in one-tenth of a 1-3-mm fibre segment, with the remainder of each segment pooled with fibre segments of the same type (I or II) for subsequent protein quantification by western blotting. This method, which we validated using standard western blotting, is much simpler and cheaper than previous methods and is adaptable for laboratories routinely performing biochemical analyses. Use of dot blotting for fibre typing will facilitate investigations of fibre-specific responses to diverse stimuli, which will advance our understanding of skeletal muscle physiology and biochemistry.
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