. 2023 Jan 9;53(3):595–613. doi: 10.1007/s40279-022-01805-w

Table 1.

Summary of studies that have altered critical power (CP) via chronic or acute interventions

Study	Population	Mode	Intervention	Effect on CP	Physiological effects of intervention	CP determination method
Moritani et al. [21]	H (2)	Upright cycling	Hypoxia (FiO₂ = 0.09)	↓ CP (106 vs 214 W)		4CWR
Gaesser and Wilson [158]	ETM (2) HM (3)	Upright cycling	Endurance training (6 weeks)	↑ CP (228 vs 201 W)	↔ $\dot{V}$ O_2peak	4CWR
Gaesser and Wilson [158]	ETM (3) HM (3)	Upright cycling	HIIT (6 weeks)	↑ CP (254 vs 220 W)	↑ $\dot{V}$ O_2peak	4CWR
Poole et al. [159]	HM (8)	Upright cycling	HIIT (7 weeks)	↑ CP (288 vs 325 W)	↑ $\dot{V}$ O_2peak, ↑LT	5CWR
Jenkins and Quigley [160]	HM (12)	Upright cycling	Endurance training (8 weeks)	↑ CP (255 vs 196 W)	↑ $\dot{V}$ O_2peak	3CWR
Hill [161]	HM (13) HF (11)	Upright cycling	Cadence (100 rpm vs 60 rpm)	↓ CP (195 vs 207 W)		4CWR
Serres et al. [162]	COPD (8)	Upright single leg knee extension	Endurance training (3 weeks)	↑ CP (1.8 vs 1.3 kg.s⁻¹)	↑ $\dot{V}$ O_2peak, ↑MVC	3CWR
Puente-Maestu et al. [38]	COPDM (27)	Upright cycling	Endurance training (6 weeks)	↑ CP (65 vs 58 W)	↑ $\dot{V}$ O_2peak, ↓peak blood [La], ↓ $\dot{V}$ e_peak	3CWR
Barker et al. [163]*	ETM (5) ATM (6)	Upright cycling	Cadence (100 rpm vs 60 rpm)	↓ CP (189 vs 297 W)		4CWR
Vanhatalo et al. [164]	HM (8) HF (1)	Upright cycling	HIIT (4 weeks)	↑ CP (255 vs 230 W)	↑ $\dot{V}$ O_2peak, ↑GET	3MT
Miura et al. [165]	HM (6) HF (2)	Upright cycling	Heavy priming exercise	↑ CP (177 vs 169 W)		4CWR
Vanhatalo et al. [37]	HM (7)	Prone knee extension	Hyperoxia (FiO₂ = 0.7)	↑ CP (18 vs 16 W)	↓Rate of change: muscle [ADP], [PCr], [Pi], pH; ↑τ_PCr, ↑Δ[HbO₂], ↓Δ[HHb], ↑TOI, ↑TD_[HHb], ↔ τ_[HHb]¹	4CWR
Corn and Barstow [166]	HM (7)	Upright cycling	N-acetylcysteine (acute oral supplementation)	↑ CP (232 vs 226 W)	↑GSH, ↑EMG_MPF (RF), ↓EMG_RMS (VL)	4CWR
Dekerle et al. [56]	HM (5) HF (6)	Upright cycling	Hypoxia (FiO₂ = 0.15)	↓ CP (190 vs 220 W)	↓SaO₂	3–4CWR
Valli et al. [61]	HM (4) HF (2)	Upright cycling	Hypoxia (altitude = 5050 m)	↑ CP (123 vs 81 W)	↓ $\dot{V}$ O2_peak, ↓blood [lactate], ↓SaO₂, ↓O₂ pulse	3 CWR
Broxterman et al. [73]	HM (8)	Handgrip	Duty cycle (50% vs 20%)	↓ CP (3.9 vs 5.1 W)	↓Q̇_BA, ↑iEMG, ↓EMG_MPF, ↓m $\dot{V}$ O₂, ↔ [THb], ↓end-exercise [HHb] ²	3–4CWR
Mueller et al. [167]	ETM (11)	Upright cycling	Resistance + vibration training (8 weeks)	↑ CP (296 vs 286 W)	↑Capillary:fibre, ↑thigh LBM, ↑MyHC1 and ↑MyHC2 CSA, ↔ SDH	4CWR
Broxterman et al. [168]*	ETM (5) ATM (5)	Upright cycling	Cadence (100 rpm vs 60 rpm)	↓ CP (196 vs 214 W)		4 CWR
Black et al. [169]	HM (10)	Upright cycling	Pacing (self vs constant load)	↑ CP (265 vs 250 W)	↓ ${MRT}_{\dot{V} O 2}$ , ↑VO₂ in first 60 s	3–4TT/3–4CWR
Broxterman et al. [75]	HM (6)	Handgrip	Blood flow occlusion	↓ CP (-0.7 vs 4.1 W)	↓EMG_RMS, ↑[HHb], ↓[HbO₂], ↓[THb]²	4CWR
Parker-Simpson et al. [60]	HF (13)	Upright cycling	Hypoxia (FiO2 = 0.13)	↓ CP (132 vs 175 W) ↓ EP (134 vs 172 W)	↓ $\dot{V}$ O2_max	5CWR and 3MT
Deb et al. [170]	ETM (11)	Upright cycling	Hypoxia (FiO₂ = 0.145) ± sodium bicarbonate	↓ CP (265 vs 263 vs 301 W)	↓SaO₂	3MT
Goulding et al. [114]	HM (10)	Supine cycling	Heavy priming exercise	↑ CP (185 vs 177 W)	↓ $τ_{\dot{V} O 2}$ , ↔ $\dot{V}$ O_2max, ↑[HbO₂], ↑τ_[HHb]¹	4CWR
Townsend et al. [63]	ETM (9)	Upright cycling	Hypoxia (FiO₂ = 0.18, 0.159, 0.14, 0.123)	↓ CP (257, 235, 218, 196 vs 270 W)		3TT
Clark et al. [171]	ETM (6)	Upright cycling	2 h heavy exercise	↓ CP (282 vs 306 W)		3MT
Goulding et al. [117]	HM (8)	Supine cycling	Exercise transition from elevated baseline	↓ CP (132 vs 146 W)	↑ $τ_{\dot{V} O 2}$ , ↔ $\dot{V}$ O2_max, ↔ [HbO₂], ↑τ_[HHb], ↓Δ[HHb]/Δ $\dot{V}$ O₂³	4CWR
Goulding et al. [130]	HM (7)	Upright cycling	Exercise transition from elevated baseline	↓ CP (203 vs 213 W)	↑ $τ_{\dot{V} O 2}$ , ↑ [HbO₂], ↑ τ_[HHb], ↓Δ[HHb]/Δ $\dot{V}$ O₂¹	4CWR
La Monica et al. [62]	HM (21)	Upright arm cycling	Hypoxia (FiO₂ = 0.14)	↓ CP (85 vs 90 W)	↓ $\dot{V}$ O_2peak	4CWR
Mitchell et al. [86]	ETM (21)	Upright cycling	SIT, SIT + blood flow restriction (4 weeks)	↑ CP (302, 302 vs 292 W)	↑ $\dot{V}$ O_2peak, ↔ capillarity, ↔ mitochondrial protein content	3-5CWR
Clark et al. [172]	HM (14)	Upright cycling	2 h heavy exercise	↓ CP (CWR: 256, EP: 256 vs EP: 287 W)	↓Muscle [glycogen], ↔ $\dot{V}$ O_2peak	4CWR and 3MT
Clark et al. [173]	ETM (16)	Upright cycling	2 h heavy exercise	↓ CP (236 vs 260 W)	↓Muscle [glycogen], ↔ $\dot{V}$ O_2peak	3MT
Goulding et al. [64]	HM (8)	Supine cycling	Hyperoxia (FiO₂ = 0.5)	↑ CP (148 vs 134 W)	↑ $\dot{V}$ O_2max, ↓ $τ_{\dot{V} O 2}$ , ↑[HbO₂], ↔ τ_[HHb] ³	4CWR
Morgan et al. [152]	HM (16)	Upright cycling	Acetaminophen (acute oral supplementation)	↑ CP (297 vs 288 W)	↑EMG_RMS, ↔ $\dot{V}$ O2_peak	3MT
Waldron et al. [174]	HM (12)	Upright cycling	Taurine (acute oral supplementation)	↑ CP (212 vs 197 W)	↑Post-exercise blood [lactate]	3MT
Goulding et al. [65]	HM (9)	Upright cycling	Hyperoxia (FiO₂ = 0.5)	↑ CP (216 vs 197 W)	↑ $\dot{V}$ O_2max, ↔ $τ_{\dot{V} O 2}$ ↑PetO₂, ↑[HbO2], ↓[HHb], ↔ τ_[HHb]³	4CWR
Goulding et al. [131]	T1DM (7)	Upright cycling	Heavy priming exercise	↑ CP (161 vs 149 W)	↓ $τ_{\dot{V} O 2}$ , ↔ $\dot{V}$ O_2max, ↔ [HbO₂], ↓ τ_[HHb] ¹	4CWR
Karabiyik et al. [175]	TM (32)	Upright cycling	SIT (4 weeks) ± hypoxia (FiO₂ = 0.135)	↑ CP (200 vs 170 W)^#	↑Post-ramp blood [lactate], ↔ $\dot{V}$ O_2peak	3MT
Collins et al. [176]	HM (5) HF (6)	Upright cycling	Endurance training (8 weeks)	↑ CP (161 vs 140 W)	↑ $\dot{V}$ O_2max	3–6CWR
Collins et al. [176]	HM (6) HF (5)	Upright cycling	HIIT (8 weeks)	↑ CP (176 vs 140 W)	↑ $\dot{V}$ O_2max	3–6CWR

Study: *latter publication uses a sub-set of data taken from the former publication

Population: AT anaerobically trained, COPD chronic obstructive pulmonary disease, ET endurance trained, F female, M male, H healthy, n number of participants, T1D type 1 diabetes

Intervention: FiO ₂ fraction of inspired O_2, HIIT high-intensity interval training, rpm revolutions per minute, SIT sprint interval training, ± with and without

Effect on CP: ↑ increased, ↓ decreased, ^#values for CP estimated from visual inspection of figures

Physiological effects of intervention (all factors considered for chronic interventions, only those factors measured during the determination of CP considered for acute interventions): ¹ [HHb], [THb], [HbO₂] determined via near infrared spectroscopy on the VL, ²[HHb], [THb], [HbO₂] determined via near infrared spectroscopy on the flexor digitorum superficialis, ³[HHb], [THb], [HbO₂] determined via near infrared spectroscopy on the VL and RF, τ_[HHb] time constant of [HHb] kinetics, $τ_{\dot{V} O 2}$ time constant of $\dot{V}$ O₂ kinetics, ADP adenosine diphosphate, CSA cross-sectional area, EMG_MPF electromyography median power frequency, EMG_RMS electromyography root mean squared, GET gas exchange threshold, HbO₂ oxygenated haemoglobin, HHb deoxygenated haemoglobin, iEMG integrated electromyography, La lactate, LBM lean body mass, LT lactate threshold, ${MRT}_{\dot{V} O 2}$ mean response time of $\dot{V}$ O₂, MVC maximal voluntary contraction, m $\dot{V}$ O₂ muscle $\dot{V}$ O₂ estimated via combined near infrared spectroscopy and doppler ultrasound, MyHC1 myosin heavy chain 1, MyHC2 myosin heavy chain 2, PCr phosphocreatine, PetO₂ end-tidal pressure of O₂, Pi inorganic phosphate, Q̇_BA brachial artery blood flow, RF rectus femoris, SaO₂ arterial oxygen saturation, SDH succinate dehydrogenase, THb total haemoglobin, $\dot{V}$ e_peak highest ventilation measured, VL vastus lateralis, $\dot{V}$ O₂ rate of oxygen uptake, VO₂ total oxygen consumed, $\dot{V}$ O_2max maximal $\dot{V}$ O₂ recorded following verification from additional trials > CP, $\dot{V}$ O_2peak highest $\dot{V}$ O₂ recorded but not verified with additional tests > CP, ↔ unchanged

CP determination method: 3MT 3-min all-out test, nCWR number of constant work-rate trials, nTT number of time trials