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Urology & Nephrology Open Access Journal

Review Article Volume 7 Issue 5

Physical activity and prostate cancer: a systematic review

Abdalla Ali Deb,1 Chidiebere Emmanuel Okechukwu,2 Shady Emara,3 Sami A Abbas4

1Locum Consultant Urologist NHS- UK
2Physical activity and health promotion, Department of Biomedicine and prevention, Faculty of Medicine and Surgery, University of Rome Tor vergata. Rome, Italy
3Clinical Fellow in Urology, Western General Hospital UK
4Consultant Urologist, National Institute of Urology and Nephrology Cairo; Egypt

Correspondence: Abdalla Ali Deb, Locum Consultant Urologist NHS- UK

Received: October 06, 2019 | Published: October 30, 2019

Citation: Deb AA, Emmanuel O, Emara S, et al. Physical activity and prostate cancer: a systematic review. Urol Nephrol Open Access J. 2019;7(5):117-129. DOI: 10.15406/unoaj.2019.07.00258

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Abstract

Numerous studies confirmed that planned exercise therapy is a possible adjunct strategy connected with significant improvements in symptom-related results including exercise tolerance as well as several cancer patients-reported progress such as improvement in quality of life, and physical functioning during conventional adjuvant therapy. The aim of this review was to evaluate the association between physical activity and prostate cancer. Apart from lung cancer, prostate cancer is highly prevalent among men. We searched for original articles, systematic reviews, and meta-analyses that reported on exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. The following electronic databases was used: PubMed, Science Direct, Medline, Sports Discus, Web of Science, Google Scholar and Cochrane database. 85 studies written in English were included in this review. Patient’s cardio-metabolic profile, type of exercise, specific workloads, frequency, duration, intensity and safety precautions are factors to consider when scheduling an exercise program. Regular participation in physical activity is important in the prevention of prostate cancer and it is associated with positive treatment outcomes in patients undergoing Androgen deprivation therapy. Physical Activity may affect prostate cancer progression by reducing insulin resistance, decreasing bioavailable Insulin-like growth factor 1 (IGFI), increasing adiponectin levels and circulating levels of insulin. Interleukin 6 (IL-6) promotes cell proliferation and inhibits apoptosis of prostate cancer cells in vitro. Physical activity is associated with lower circulating IL-6. Based on the information examined in this study, physical activity may be an effective nonpharmacological means in the treatment of prostate cancer.

Keywords: physical activity, exercise, prostate tumor, cancer prevention

Introduction

For the past 2 decades, improved research and clinical attention has focused on the effectiveness of exercise therapy as an adjunct approach for the treatment of cancer.1 Randomized trials validate that planned exercise therapy is a feasible adjunct tactic connected with significant improvements in symptom-related outcomes including exercise tolerance as well as multiple patient-reported treatment progress such as improvement in quality of life and physical functioning equally during conventional adjuvant therapy.2 In this review, we outline relevant studies related to exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. Prostate cancer is the second most prevalent form of cancer diagnosed among men after lung cancer.3 Androgen deprivation therapy (ADT) is applied in the treatment of patients in the advanced stage of prostate cancer. The side effects of ADT include erectile dysfunction,4 increase fat mass,5 and reduction in muscle strength.6 Combined resistance and aerobic exercise training program was effective in reversing muscle loss in men undergoing ADT due to prostate cancer.7 Pelvic floor/sphincter training is effective in plummeting incontinence in patients with prostate cancer.8,9 The molecular mechanisms behind the positive effects of exercise training programs in addition to ADT has not been well understood, however there was a decrease in inflammation due to low nuclear factor-κB activation in LNCaP cells incubated with post-exercise serum10 and suppressed growth and increased apoptosis of LNCaP cells incubated with post-exercise serum.11 Exercise alters p53, p21 and caspase activities resulting in tumour growth inhibition, tumour apoptosis, tumour suppression and suppressed metastasis.12,13 Physical activity was effective in reducing prostate carcinogenesis in transgenic model.14 The demonstration of possible mechanisms whereby exercise alters the progression of carcinogenesis might strengthen the clinical outcome of cancer treatment.

Exercise could also result to reductions in obesity and oxidative stress and a modulation of immune responses in prostate cancer patients.15 Exercise causes reductions in circulating levels of testosterone and insulin-like growth factors16,17 therefore reducing the development and spread of neoplastic cells. Apart from exercise, testosterone levels are controlled by diet,18 and this may contribute to variances in exercise response among various populations.19 The aim of this review was to evaluate the association between physical activity and prostate cancer. In this review, we outlined relevant studies concerned about exercise-mediated changes in prostatic growth and progression from 1980 to 2018. These mediated changes are linked to the role of consistent physical activity in improving the quality of life, physical fitness and averting the progression of prostate cancer among individuals diagnosed of prostate cancer.

Methods

Search strategy

We searched for studies that reported on exercise-mediated changes in the prostatic tumour risk and progression from 1980 to 2018. The following electronic databases was used: PubMed, Science Direct, Medline, Sports Discus, Web of Science, Google Scholar and Cochrane database. The following search strategy was modified for the various databases and search engines: Prostate cancer, exercise, physical activity, cancer, prostate tumour, cancer prevention, and cancer adjunct therapy. We assessed Full articles and extracted relevant data. We used the MeSH system to extract relevant research studies indexed in PubMed.

Types of studies

Original articles, systematic reviews, and meta-analyses.

Inclusion and exclusion criteria

We selected precise articles that described physical activity and prostate growth, exercise therapy in support of the clinical treatment of prostate cancer and exercise prescription for prostate cancer patients. The selected articles were all written in English. Articles that were not precise, uncertain and with doubtful experimental procedure were excluded. 85 studies were included in this review.

Data extraction and management

We designated all trials retrieved from the databases. We reviewed for relevance based on physical activity and prostate cancer progression, cancer prevention, exercise therapy for prostate cancer patients undergoing ADT and radiotherapy. We retrieved full-text copies of all the articles recognised as hypothetically relevant in this review. Data was reported in a narrative and concise manner. The selection process was elucidated in a Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) flow diagram (Figure 1).

Figure 1 Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) flow diagram

The effectiveness of exercise prescription and dosing for patients diagnosed with prostate cancer

Patient’s cardio-metabolic profile, type of exercise, specific workloads, frequency, duration, intensity and safety precautions are factors to consider when planning an exercise program. Regular involvement in physical activity is vital in the prevention of prostate cancer and it is connected with positive treatment results in patients undergoing ADT.20 Patients diagnosed with prostate cancer should accumulate at least; 150 min per week of moderate-intensity aerobic exercise or 75 min per week of vigorous aerobic exercise, or both, this is in accordance with the reference exercise strategies prescribed by the American College of Sports Medicine (ACSM) for cancer patients.21,22 Cardiovascular diseases are the leading cause of death in men with prostate cancer23 and exercise performed according to the standard prescription improves cardiovascular fitness and averts cardiovascular deaths.24 Galvao et al.25 found a significant increase in muscle strength in prostate cancer patients allocated to the group that took part in chest press, a significant increase in muscle stamina was detected in the group that participated in chest press, there was significant increase in Muscle thickness at the quadriceps position. There was substantial development in general cardiovascular fitness, flexibility, muscle strength, quality of life, and drastic reduction in fatigue among prostate cancer patients undertaking radiotherapy after undergoing an 8-week cardiovascular exercise-training program.26 A randomised controlled trial conducted by Segal et al.27 in which Prostate cancer patients completed resistance exercise training 3 times per week, demonstrated global progresses in quality of life, muscular strength, body fat ratio decrease and lessening in fatigue in the group that partook in resistance exercise and are undertaking radiotherapy, both aerobic and resistance training was found to lessen fatigue. A personalized exercise-training program planned and prescribed according to patients’ cardio-metabolic and functional capacity might be more effective in the treatment of prostate cancer.28 The ideal approach and dosage of exercise for patients diagnosed of prostate cancer has not been established.

Selected studies on physical activity and prostate cancer

According to the World Health Organization (WHO), physical activity is any physical movement produced by skeletal muscles that involves energy expenditure.29 Based on experimental and clinical studies, physical activity averts the progression of prostate cancer by changing molecular mechanisms resulting to the suppression of tumour growth. In tabulating available epidemiological facts, we categorized them by type of study (cross-sectional, prospective cohort, or case–control) and by findings (an adverse effect, no clear response, a positive trend), and a statistically significant decrease of risk in the more active individuals. There have been many cross-sectional or cohort studies relating occupation to the risk of prostate cancer (Table 1). Leisure-time physical activity have also been linked with the risk of developing prostate cancer based on cohort studies (Table 2). Four retrospective and cohort studies of sport involvement and fitness realization was critically analysed (Table 3)., two of these information found no benefit from sport involvement,70 but Wannamethee et al.64 noted a considered outcome on the reported frequency of sport participation, However, the fourth report observed that a beneficial effect was connected with a high-attained level of aerobic fitness.71

Author

Sample

Activity measure

Outcome

Comments

Cohort studies

Negative findings

Hartman et al.30a

29,133 male smokers, aged 50–69 years followed for an average of 6.1 years; 317 incident cases of PC

Self-report, sedentary job vs. occupational walkers vs. walkers/lifters vs. heavy laborers

RR 1.0, 0.6, 0.8, 1.2 (ns) of prostate cancer as stated by Finnish cancer registry

Attuned for age, urban living, smoking, benign prostate hyperplasia

Johnsen et al.31a

127,923 men, aged 20–97 years, followed for 8.5 years; 2458 cases of PC

Two classifications by interview or questionnaire: sitting, standing, or manual work; inactive, moderately inactive, moderately active, active

Occupational activity not significantly related to PC (OR manual 0.90 (0.77–1.04), p =0.15 for trend)

Attuned for leisure activity, height, weight, marital status, education

Nielsen et al.32a

22,895 Norwegian men aged 40 to >80 years followed for 9.3 years; 644 cases of PC

Modest binary classification (high vs. low level of occupational activity)

No effect of occupational activity ((high RR 1.04 (0.82–1.32); augmented risk in high vs. low education, RR 1.50 (1.11–2.19)

Age-adjusted relative risks

Putnam et al.33a

101 cases of PC were conveyed to State register office,1572 initially cancer-free men aged 40–86 years, followed for 4 years

Very energetic, ascetically active, or inactive at work, based on work-related codes

PC unrelated to occupational activity (RR for very active 1.0 (0.6–1.8))

Adjusted for age

Zeegers et al.34a

58,279 men aged 55–69 years, 1386 cases of PC over 9.3 years of follow-up

Work-related activities (estimated energy expenditure, sitting time for longest held and for most recent job)

RRs longest held: >12 vs. <8 kJ/min 0.91 (0.70–1.18) Sitting <2 vs. >6 h/day1.16 (0.91–1.47)

Attuned for age, alcohol drinking, BMI, energy intake, family history, education

Positive trend

Grotta et al.35a

13,109 Swedish men, initially aged 55 years, surveyed for 13 years; 904 cases of PC

Low vs medium vs. high level of work-related activity

HR for high activity 0.81 (0.61–1.07, ns), medium 0.96 (0.77–1.20)

Attuned for age, education, smoking, BMI, alcohol consumption, diabetes mellitus

Hrafnkelsdóttir et al.36a

24-year follow-up of 8221 Icelandic men initially aged 33–79 years; 1052 cases of PC

Work includes mostly sitting vs standing vs on the move

HR 1.0, 0.97 (0.80–1.17), 0.91 (0.79–1.06), ns

Attuned for age, height, BMI, diabetes, family history, education, medical check-ups

Significant positive findings

Clarke et al.37a

5377 men firstly, aged 25–75 years surveyed for 17–21 years; 201 cases of PC

Very active vs. sedentary

RR for inactive 1.75 (1.12–2.67), p=0.05 for trend (outcome larger in African Americans)

Attuned for age, education, ethnicity, family history

Norman et al.38

3 cohorts containing 43,836, 28,702, and 19,670 cases of PC

Work-related designations (inactive, medium, to very high level of activity)

RR for sedentary vs. high/very high groups 1.11, 1.10, and 1.11 (p=0.0001 for all three groups)

Attuned for age, year of follow-up, area of residence

Orsini et al.39a

45,887 men aged 45–79 years, surveyed for 8 years; 2735 incident cases of PC

4 categories of occupation (mostly sitting vs. heavy manual)

RR=0.72 (0.57–0.90); p=0.007 for trend; effects smaller for advanced and fatal cancers

Attuned for leisure activity, age, smoking, alcohol consumption, education, diet, energy intake, waist/hip ratio, diabetes mellitus

Parent et al.40a

449 incident cases of PC; aged 59 years

High vs. medium vs. low lifetime occupational activity, metabolic equivalents (METs)

OR intermediate 0.64 (0.41–0.98), high 0.54 (0.31–0.95)

Data attuned for age, sex, education, ethnicity, smoking, BMI, outdoor activities

Vidarsdottir et al.41

60,194 men initially aged 20–64 years followed for 23 years

Educational level (basic, medium, high)

SIR basic =0.92 (0.84–0.99), academic =1.17 (1.05–1.30)

Greater diagnosis in highly educated group

Case–control studies

Adverse findings

Negative findings

Doolan et al.42

1436 cases of PC aged 39–70 years, 1349 coordinated controls

Finnish occupation background, physical capacity classified by tertiles

OR highest tertile workload 1.15 (0.95–1.40), ns

Attuned for age, family history, economic resources

Hosseini et al.43

137 cases of PC, 137 locality controls, men <70 to >80 years

Walking to work (<10 vs. >10 h/week), intensity of work (sedentary/moderately active vs. highly active)

OR 0.7 (0.4–1.2) for longer walk (ns), OR=6.7 (1.3–35.1) for highly active work (p=0.02)

Multivariate adjusted

Lacey et al.44a

258 cases of PC, 471 age-matched controls, aged 50–94 years

Sedentary, moderate, or high work-related energy expenditures at ages 20–29 years, 40–49 years, or 12 years ago

RR 1.1 (0.7–1.7), 1.3 (0.8–1.9), 0.9 (0.5–1.8) of high vs. sedentary group

Attuned for age, marital status, education, BMI, energy intake, waist/hip ratio

Sass-Kortak et al.45

760 PC cases aged 50–84 years, 1632 telephone book controls

Quartiles of lifetime work-related activity

Active vs. least active workers OR 1.33 (1.02–1.74), p=0.18 for trend)

Attuned for age, family history, sunlight exposure

No effect

Friedenreich et al.46a

988 cases of PC, histologically confirmed, 1063 population controls

Energy expenditure <74.2 vs. >161.9 MET h/week

OR 0.90 (0.60–1.22), ns

Attuned for age, region, education, BMI, waist/hip ratio, energy intake, alcohol drinking, family and medical history

Positive trend

Lagiou et al.47

320 histologically confirmed cases pf PC aged <60 to >80 years, 246 hospital controls

Low, medium, high level of job-related activity

OR low =1.0, medium =0.95 (0.49–1.84), high =0.69 (0.40–1.22), ns

Attuned for age and education

Wiklund et al.48a

1449 incident cases of PC in men aged 35–79 years, 1118 population controls

METs h/day of lifetime work-related activity, <11.8, <14.8, <19.8, >19.8

OR 1.0, 0.81 (0.65–1.08), 0.87 (0.66–1.15) 0.84 (0.61–1.15), ns

Attuned for age, region, education, BMI, alcohol consumption, family history, diabetes mellitus, energy intake

Significant positive findings

Bairati et al.49

64 cases of PC, 5456 cases of benign prostate hyperplasia aged >45 years

(a) inactive job or light work; (b) 0, 1–49%, >50% of profession spent in inactive or light work

(a) OR 2.0 (1.1–3.6); 1.0, 1.7 (0.8–3.2), OR 2.8 (1.3–6.0) (p=0.007 for trend)

Attuned for age, education, total energy intake, smoking, use of vitamin supplements

Krishnadasan et al.50

362 cases of PC, 1805 matched controls; age not specified

Low vs. moderate vs. high work-related energy outflow

OR high 0.63 (0.40–1.00), moderate 0.96 (0.7–1.3), p=0.06 for trend)

Attuned for matching variables, pay, trichloroethylene exposure

Pierotti et al.51a

1294 incident cases of PC aged <75 years and 1451 hospital controls

3-level categorization of work-related activity at ages 12, 15–19, 30–39, and 50–59 years

OR age 12 years = 0.84 (0.67–1.06), age 15–19 years =0.94 (0.75–1.17), age 30–39 years =0.78 (0.63–0.97), age 50–59 years = 0.75 (0.61–0.93)

Attuned for age, test centre, education, Sex, BMI, total energy intake, smoking, alcohol consumption, family history

Strom et al.52a

176 cases of PC in Mexican Americans, 176 controls, age ~ 62 years

None/low vs. moderate/high energy demands of labour

Reduced risk in active (OR 0.46, 0.28–0.77), p=0.003)

Attuned for age, education, screening, exposure to agricultural chemicals

Villeneuve et al.53a

1623 histologically confirmed cases of PC, 1623 controls, aged 50–74 years

4-level classification of work (sitting to energetic)

Significant advantage from strenuous activity in teens or early 20 s, (OR light 0.8 (0.5–1.3), moderate 0.8 (0.5–1.2), strenuous 0.6, 0.4–0.9), ns for 30 s (0.7), 50 s, (0.8) or 2 years before interview (0.9)

Attuned for age, area of residence, smoking, alcohol consumption, BMI, diet, income, family history

Table 1 Occupational activity and the risk of developing prostate cancer
HR, hazard ratio; MET, metabolic equivalent, ns not significant; OR, odds ratio; PC, prostate cancer; PMR, proportionate mortality ratio; RR, relative risk or rate ratio; SES, socioeconomic status; SIR, standardized incidence ratio

Author

Sample

Activity measure

Findings

Comments

Cohort studies

Adverse trend

Negative findings

Crespo et al.54

9824 men initially aged 35–79 years followed for death

Framingham index (quartiles)

No association between physical activity and prostate deaths

Adjusted for age, education, urban residence, smoking, BMI

Giovannucci et al.55

47,452 health experts initially aged 40–75 years, followed for 8 years; 1362 cases of PC

Leisure activity, 1 vs. 46.8 MET h/week

No significant association to PC except idea of less metastatic activity and lower Gleeson score with vigorous intensity exercise

Attuned for age, vasectomy, diabetes mellitus, smoking, energy intake, diet

Grotta et al.35b

13,109 Swedish men, initially aged 55 years, tracked for 13 years; 904 cases of PC

Low vs. high leisure activity

HR 0.93 (0.76–1.14, ns) for incident PC if high physical activity

Attuned for age, education, smoking, BMI, alcohol drinking, diabetes mellitus

Johnsen et al.31a

127,923 men, median initial age 61 years, followed for 8.5 years; 2458 cases of PC

Quartiles of leisure activity (<25 to >71 MET h/week)

Leisure activity unrelated to incident PC

Attuned for work-related activity, height, weight, marital status, education

Lee et al.56

8922 Harvard alumni, mean age 67 years; 439 developed PC during 5 years of follow-up

Physical activity questionnaire completed twice, weekly energy expenditure quartiles (<4.2 MJ to >12.6 MJ)

PC disparate to total volume of physical activity or weekly volume of vigorous physical activity

Accustomed for age, BMI, smoking, alcohol consumption, family history

Littman et al.57

34,757 men initially aged 50–76 years; 583 cases of PC

MET h/week, walking pace, stair climbing, high-intensity activity, activity at earlier ages

No association with PC except in sub-group aged >65 years with normal body mass

Attuned for family history, BMI, income

Liu et al.58

982 cases of PC in 22,071 physicians aged 40–84 years over 11 years of follow-up

Exercise sufficient to cause a sweat <1/week. vs. >5/weeks

No relationship of frequent activity to incidence of PC

Adjusted for smoking, alcohol drinking, height, diabetes mellitus, high cholesterol, hypertension, use of multi-vitamins

Parent et al.40b

449 incident cases of PC among 3730 cancer patients

participation in sports and outdoor activities (never or not often vs. often)

No significant consequence on risk of PC

Covariates age, SES, education, ethnicity, smoking, BMI

Platz et al.59

46,786 health professionals, initially aged 40–75 years; 2896 incident cases of PC over 14 years

Vigorous leisure activity <3, >3 MET h/week

No relationship to PC

Attuned for age, family history, BMI, diabetes mellitus, smoking, diet

Putnam et al.33b

101 cases of PC in 1572 initially cancer-free men, originally aged 40–64 years, followed for 4 years

Very active, moderately active, inactive

Risk of PC unrelated to leisure activity

Attuned for total energy intake

Positive trends

Clarke et al.37b

5377 men, aged <50 to >70 years, followed for 17–21 years; 201 cases of incident or fatal PC

Much vs. moderate vs. little or none

RR much 1.00, moderate 1.10 (0.75–1.61), inactive 1.17 (0.80–1.72), ns

Attuned for age, education, ethnicity, family history

Giovannucci et al.60

47,620 health specialists, initially aged 40–75 years, 14 years of follow-up; 2892 incident cases of PC (482 advanced, 280 fatal)

Vigorous physical activity, 0 vs. >29 MET h/week

No relationship for all subjects; if >65 years, OR for advanced cancer 0.33 (0.17–0.62)

Age, BMI, smoking, height, family history, diabetes mellitus, ethnicity, non-vigorous activity, energy intake and diet

Hrafnkelsdóttir et al.36b

24 years of follow-up of 822 Icelandic men initially aged 33–79 years; 1052 cases of PC

Regular physical activity from age of 20 years vs. sedentary

HR 0.93 (0.83–1.07) for all PC in active individuals, 0.82 (0.63–1.06) for advanced cancers

Accustomed for age, height, BMI, diabetes, family history, education, medical check-ups

Nielsen et al.32b

22,895 Norwegian men, initially aged 40 to >80 years, followed for 9.3 years; 644 cases of PC

High vs. low leisure activity

RR 0.80 (0.62–1.03)

Multivariate adjusted

Moore et al.61

293,902 men initially aged 50–71 years followed for up to 8.2 years; 17,872 cases of PC

Exercise at starting point and in adolescence (never/rarely to >5 times/week)

RR of total cases 0.97 (0.91–1.03), p=0.03 for inclination supporting frequent activity during adolescence, but no relationships to exercise habits at baseline

Accustomed for age, marital status, education, smoking, medical history, BMI, waist circumference, family history, diet and supplements

Nilsen et al.62

29,110 Norwegian men, initially mean age 52 years, followed for 7 years; 957 incident cases of PC

Activity score based on frequency, intensity and duration of activity (low vs. high)

Connected to total cancer cases (RR=0.86), but for advanced cancer RR=0.64 (0.43–0.95), p=0.02 for inverse trend

Attuned for age, marital status, education, BMI, smoking, alcohol consumption

Patel et al.63

72,174 men, initial mean age 64 years; 5503 incident cases of PC over 9 years

MET h/week (<0.7–35) at age 40 years

No significant effect (but active have fewer hostile tumours, RR 0.69 (0.52–0.92), p=0.06 for trend

Accustomed for age, ethnicity, BMI, weight change, energy intake, diet and vitamin use, diabetes mellitus, family and medical history

Zeegers et al.34b

58,279 men initially aged 55–69 years; 1386 cases of PC over 9.3 years

Cycling/walking (min/day), gardening (h/week)

Gardening unrelated to PC; biking/walking <10 vs. >60 min/d, RR 0.85 (0.69–1.05), ns

Accustomed for age, alcohol drinking, BMI, energy intake, family history, gardening, sport participation

Significant positive findings

Hartman et al.30a

29,133 male smokers, initially aged 50–69 years, followed for up to 9 years; 317 cases of PC

Inactive vs, moderate/heavy leisure activity in working men

RR 0.7 (0.46–0.94) favoring active leisure

Attuned for age, urban living, smoking, benign hyperplasia

Orsini et al.39b

45,887 men, initially aged 45–79 years, followed for 8 years; 2735 incident cases of PC

Walking or cycling, 5 categories (hardly ever to >60 min/day)

RR=0.86 (0.76–0.98), p=0.028 for trend; effects greater for advanced (RR=0.74) and fatal (RR=0.72) cancers

Attuned for work-related activity, age, smoking, alcohol drinking, education, diet, energy intake, waist/hip ratio, diabetes mellitus

Wannamethee et al.64a

Potential study of 7588 men aged 40–59 years; 120 incident cases of PC

6-level classification of leisure activity from none to vigorous

Advantage from vigorous activity, OR 0.25 (0.06–0.99, p=0.06 for trend

Attuned for age, smoking, alcohol consumption, BMI, social class

Case–control studies

Adverse findings

Chen et al.65

237 cases of PC, 481 controls aged >50 years

Mainly a dietary study: 4-level categorization of physical activity

Adverse effect of high vs. moderate exercise: OR 1.84 (1.01–3.34)

Multivariate analysis (age, BMI, income, marriage, dietary variables)

Wiklund et al.48b

1449 incident cases of PC, 1118 population controls, mean age 67–68 years

MET h/day lifetime recreational activity, <7.4 to >13.5

OR <7.4=1.0, <10.2=1.33 (1.00–1.78), <13.5=1.43 (1.07–1.91), >13.5=1.56 (1.16–2.10), p=0.006 for adverse effect of active leisure

Attuned for age, region, education, BMI, alcohol consumption, family history, diabetes mellitus, energy intake

No clear effect

Lacey et al.44b

258 cases of PC, 471 age-matched controls, aged 50–94 years

Tertiles of moderate/vigorous or all physical activity at age 20–29 years, age 40–49 years, and 12 years ago

No association to PC

Attuned for age, marital status, education, BMI, energy intake, waist/hip ratio

Pierotti et al.51a

1294 incident cases of PC aged <75 years and 1451 hospital controls

3-level classification of physical activity at ages 12, 15–19, 30–39, and 50–59 years

No effect on risk of PC at any age

Accustomed for age, test center, education, SES, BMI, total energy intake, smoking, alcohol drinking, family history

Sanderson et al.66

416 incident cases of PC, 429 Medicare beneficiary controls aged 65–79 years

Tertiles of strenuous and of moderate physical activity (h/week)

No relationship to PC in either African American or Caucasian men

Adjusted for age, geographic region, family history

Strom et al.52b

176 cases of PC in Mexican Americans, 176 controls, age ~ 62 years

Leisure activity (<1/week vs. >1/week)

No effect on risk of PC

Attuned for age, education, screening, work-related activity

Villeneuve et al.53b

1623 histologically confirmed cases of PC, 1623 controls, age 50–74 years

5-level classification (<1/month to >5/week)

No clear relationship to PC

Accustomed for age, area of residence, smoking, alcohol consumption, BMI, diet, income, family history

Positive trends

Friedenreich et al.46b

988 incident cases of PC, 1063 population controls, mean age 67 years

<78.5 vs. >25.1 MET h/week

OR 1.00, 0.80 (0.61–1.04), p=0.06 for trend

Accustomed for age, region, education, BMI, waist/hip ratio, energy intake, alcohol drinking, family and medical history

Significant positive findings

Darlington et al.67

752 cases from Ontario cancer registry aged 50–84 years, telephone listing controls

Strenuous activity mid-teens, early 30 s, early 50 s (yes/no)

OR for strenuous activity in teens =1.0 (0.8–1.2), early 30 s=0.9 (0.7–1.0), early 50 s=0.8 (0.6–0.9).

Attuned for age, education, BMI, family history, occupation

Jian et al.68

130 histologically confirmed cases of PC, 274 controls, aged <65 to >75 years

Reported MET hours of moderate and total activity (<40 vs >120; <44 vs. >135)

OR moderate activity <40=1.0, <80=0.47 (0.22–1.02), <120=0.46 (0.21–0.99), >120=0.20 (0.07–0.62), p=0.015, Total activity <44=1.0, <90=0.42 (0.18–0.99), <135=0.36 (0.16–0.86), >135=0.39 (0.15–0.99), p=0.50 for trend)

Accustomed for age, area of residence, education, salary, marital status, number of children, years in labour force, family history, BMI, energy intake

Yu et al.69

1162 cases of PC; 3124 matched hospital controls, age <45 to >75 years

Leisure activity (active, moderate, or seldom)

Risk higher in sedentary (OR seldom = .3 (1.0–1.6), moderate = 1.1 (0.9–1.3) active = 1.0 (p=0.03)

Attuned for age

Table 2 Leisure-time physical activity and the risk of developing prostate cancer
BMI, body mass index; HR hazard ratio; MET, metabolic equivalent; ns non-significant; NHANES, National Health and Nutrition Examination Survey; OR, odds ratio; PC, prostate cancer; RR, relative risk; SES, socioeconomic status

Author

Sample

Activity measure

Findings

Comments

Cohort studies

Merrill et al.70

PSA levels of 536 partakers in senior citizen games aged >50 years

Years active >3 times/week

Total physical activity unrelated to PSA levels

Attuned for age

Wannamethee et al.,64b

Potential study of 7588 men aged 40–59 years; 120 incident cases of PC

Sporting activity (none, >1/month, >1/week, >2/week)

RR none =1.00, <1/month =0.98, >1/month to 1/week =0.63, >2/week =0.53, p=0.05

Attuned Age, smoking, alcohol, BMI, SES

Zeegers et al.34c

58,279 men aged 55–69 years; 1386 cases of PC over 9.3 years

Sport involvement (never/ever; frequency; duration, year)

Sport involvement unrelated to PC

Attuned for age, alcohol consumption, BMI, energy intake, family history, education

Case-control studies

Hållmarker et al.72

185,412 partakers in Vasaloppet ski contest and 184,617 non-participants

1827 vs. 1435 cases PC

HR 1.22 (1.13–1.30) backing non-participants

Non-participants matched for age, sex, county of residence

Galvão73

57 prostate cancer patients, aged 70.0±8.4 year

Randomized to multimodal supervised aerobic, resistance, and flexibility exercises undertaken thrice weekly (exercises (EX); n=28) or usual care (care controls (CON); n=29) for 3 months. 

A significant difference between groups for self-reported physical functioning (3.2 points; 95% confidence interval, 0.4–6.0 points; P=0.028) and lower body muscle strength (6.6 kg; 95% confidence interval, 0.6–12.7; P=0.033) at 3 months favouring EX.

With bone metastases

Table 3 Sports involvement, attained aerobic fitness, and risk of prostate cancer
BMI, body mass index; HR, hazard ratio; ns non-significant; PC, prostate cancer; PSA, prostate serum antigen; RR, relative risk; SES, socioeconomic status; EX, exercises

Possible biological mechanisms linking exercise and prostate cancer

EL Richman et al.74 Observed that walking pace was related to a lesser risk of prostate cancer independently of walking period, they stated that men who walked 3 or more hours/week at a brisk pace had a 57% lower risk of prostate cancer. Physical Activity may affect prostate cancer progression by reducing insulin resistance, decreasing bioavailable Insulin-like growth factor 1 (IGFI), increasing adiponectin levels and circulating levels of insulin75 (Figure 2). Interleukin 6 (IL-6) promotes cell proliferation and inhibits apoptosis of prostate cancer cells in vitro;76 however, physical activity is associated with lower circulating IL-6.77 There is an increase in tumor blood flow in animal models, during intense endurance exercise, due to the change in vasculature, thus causing an upsurge in tumor perfusion and oxygenation and in turn decreases the propensity for metastasis.78 Regulation of tumor vasculature might be a likely biological mechanism through which exercise prevents prostate cancer progression. Elevated serum levels of IGF-1, leptin and insulin are related to higher risk of prostate cancer progression.79,80 LNCaP cells cultured with post exercise serum, expresses reduction in cell proliferation and increased apoptosis.81

Figure 2 Possible Biological mechanisms linking Physical activity and Prostate Cancer

Exercise lessens the side effects associated with androgen deprivation treatment for Prostate cancer.82 Aerobic exercise exerts cardio-protective effects in animal-subjected to ADT.83 Exercise results to an upsurge in the production of sex hormone–binding globulin (SHBG), dropping testosterone levels.84 Exercise boost antioxidant-enzyme repair mechanisms and drops lipid peroxidation levels, in turn plummeting free radicals and minimizing oxidative stress.85 Regular physical activity combined with lifestyle adjustment and exogenous natural supplements in addition to the pharmacological, surgical and radiotherapeutic treatment of prostate cancer may enable clinicians to attain the anticipated treatment goal.

Conclusion

Based on the information obtained and analysed in this study, a practical exercise and activity goal personalized for prostate cancer patients to increase their chances of survival would be a multidimensional tactic to decrease central adipose tissue deposition and to lessen circulating levels of inflammation, insulin, and unfavourable sex hormones. Further studies aimed to assess the most effective exercise therapy and actual dose, personalised according to patients’ clinical status for averting prostate cancer progression are vital in order to develop a comprehensive prevention and treatment goal for prostate cancer. Physical activity levels, ranging from walking to more intense activities and exercise routines, offers unique benefits. data from Randomized trials continue to accumulate regarding the positive effects of exercise on treatment outcomes for men with prostate cancer and the implementation of exercise during and after treatment for prostate cancer ought to be part of the standard of care and treatment goal. The radiation oncologists are provided with exceptional chance to restate healthy lifestyle methods and modifications owing to the extensive time spent with patients on a weekly basis during treatment. Prostate cancer treatment is one of the lengthiest treatment regimens, and the oncologist is given several opportunities to recommend and aid to implement exercise and lifestyle changes.

Acknowledgements

None.

Funding details

None.

Conflicts of interest

The author declares there is no conflict of interest.

References

  1. Friedenreich CM, Woolcott CG, McTiernan A, et al. Alberta physical activity and breast cancer prevention trial: Sex hormone changes in a year-long exercise intervention among postmenopausal women. J Clin Oncol. 2010;28(9):1458–1466.
  2. Scott JM, Zabor EC, Schwitzer E, et al. Efficacy of exercise therapy on cardiorespiratory fitness in patients with cancer: A systematic review and meta-analysis. J Clin Oncol. 2018;36(22):2297–2305.
  3. Quinn M, Babb P. Patterns and trends in prostate cancer incidence, survival, prevalence and mortality, I: international comparisons. BJU Int. 2002;90(2):62–173.
  4. Zelefsky MJ, Eid JF. Elucidating the etiology of erectile dysfunction after definitive therapy for prostate cancer. Int J Radiat Oncol Biol Phys. 1998;40(1):129–133.
  5. Smith MR, Finkelstein JS, McGovern FJ, et al. Changes in body composition during androgen deprivation therapy for prostate cancer. J Clin Endocrinol Metab. 2002;87(2):599–603.
  6. Taylor LG, Canfield SE, Du XL. Review of major adverse effects of androgen deprivation therapy in men with prostate cancer. Cancer. 2009;115(11):2388–2399.
  7. Galvao DA, Taaffe DR, Spry N, et al. Combined resistance and aerobic exercise program reverses muscle loss in men undergoing androgen suppression therapy for prostate cancer without bone metastases: a randomized controlled trial. J Clin Oncol. 2010;28(2):340–347.
  8. Filocamo MT, Li Marzi V, Del Popolo G, et al. Effectiveness of early pelvic floor rehabilitation treatment for post-prostatectomy incontinence. Eur Urol. 2005; 48(5):734–738.
  9. Overgard M, Angelsen A, Lydersen S, et al. Does physiotherapist-guided pelvic floor muscle training reduce urinary incontinence after radical prostatectomy? A randomized controlled trial. Eur Urol. 2008;54(2):438–448.
  10. Soliman S, Aronson WJ, Barnard RJ. Analyzing serum-stimulated prostate cancer cell lines after low-fat, high-fiber diet and exercise intervention. Evid Based Complement Altern Med. 2011;2011:529053.
  11. Rundqvist H, Augsten M, Stromberg A, et al. Effect of acute exercise on prostate cancer cell growth. PLoS One. 2013;8(7): e67579.
  12. Leung PS, Aronson WJ, Ngo TH, et al. Exercise alters the IGF axis in vivo and increases p53 protein in prostate tumor cells in vitro. J Appl Physiol. 2004;96(2):450–454.
  13. Barnard RJ, Leung PS, Aronson WJ, et al. A mechanism to explain how regular exercise might reduce the risk for clinical prostate cancer. Eur J Cancer Prev. 2007;16(5):415–421.
  14. Esser KA, Harpole CE, Prins GS, et al. Physical activity reduces prostate carcinogenesis in a transgenic model. Prostate. 2009;69(13):1372–1377.
  15. Shephard RJ, Shek PN. Associations between physical activity and susceptibility to cancer. Sports Medicine. 1998;26(5):293–315.
  16. Wekesa A, Harrison M, Watson RW. Physical activity and its mechanistic effects on prostate cancer. Prostate Cancer Prostatic Dis. 2015;18(3):197–207.
  17. Wheeler GD, Wall SR, Belcastro AN, et al. Reduced serum testosterone and prolactin levels in male distance runners. JAMA. 1984; 252(4):514–516.
  18. Hämäläinen EK, Adlercreutz H, Puska P, Pietinen P. Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem. 1983;18(3):369–370.
  19. Sung JF, Lin RS, Pu YS, et al. Risk factors for prostate carcinoma in taiwan: A case–control study in a chinese population. Cancer. 1999;86(3):484–491.
  20. Davies NJ, Batehup L, Thomas R. The role of diet and physical activity in breast, colorectal and prostate cancer survivorship: a review of the literature. Br J Cancer. 2011;105(1):S52–S73.
  21. Kushi LH, Doyle C, McCullough M, et al. American Cancer Society guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin. 2012;62(1):30–67.
  22. Schmitz KH, Courneya KS, Matthews C, et al. American College of Sports Medicine roundtable on exercise guidelines for cancer survivors. Med Sci Sports Exerc. 2010;42(7):1409–1426.
  23. Ketchandji M, Kuo YF, Shahinian VB, et al. Cause of death in older men after the diagnosis of prostate cancer. J Am Geriatr Soc. 2009;57(1):24–30.
  24. Pate RR, Pratt MP, Blair SN, et al. Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA. 1995;273(5):402–407.
  25. Galvao DA, Nosaka K, Taaffe DR, et al. Resistance training and reduction of treatment side effects in prostate cancer patients. Med Sci Sports Exerc. 2006;38(12):2045–2052.
  26. Monga U, Garber SL, Thornby J, et al. Exercise prevents fatigue and improves quality of life in prostate cancer patients undergoing radiotherapy. Arch Phys Med Rehabil. 2007;88(11):1416–1422.
  27. Segal RJ, Reid RD, Courneya KS, et al. Resistance exercise in men receiving androgen deprivation therapy for prostate cancer. J Clin Oncol. 2003;21(9):1653–1659.
  28. Demark WW, Clipp EC, Lipkus IM, et al. Main outcomes of the FRESH START trial: a sequentially tailored, diet and exercise mailed print intervention among breast and prostate cancer survivors. J Clin Oncol. 2007;25(19):2709–2718.
  29. World Health Organization (WHO). Global Strategy on Diet, Physical Activity and Health. 2004. p. 1–21.
  30. Hartman TJ, Albanes D, Rautalahti M, et al. Physical activity and prostate cancer in the alpha-tocopherol, beta-carotene (atbc) cancer prevention study (finland). Cancer Causes Control. 1998;9(1):11–18.
  31. Johnsen NF, Tjønneland A, Thomsen B, et al. Physical activity and risk of prostate cancer in the european prospective investigation into cancer and nutrition (epic) cohort. Int J Cancer. 2009;125(4):902–908.
  32. Nilsen TL, Johnsen R, Vatten L. Socio-economic and lifestyle factors associated with the risk of prostate cancer. Br J Cancer. 2000;82(7):1358–1363.
  33. Putnam SD, Cerhan JR, Parker AS, et al. Lifestyle and anthropometric risk factors for prostate cancer in a cohort of iowa men. Ann Epidemiol. 2000;10(6):361–369.
  34. Zeegers MP, Dirx MJ, van den Brandt PA. Physical activity and the risk of prostate cancer in the netherlands cohort study, results after 9.3 years of follow-up. Cancer Epidemiol Biomarkers Prev. 2005;14:1490–1495.
  35. Grotta A, Bottai M, Adami H-O. Physical activity and body mass index as predictors of prostate cancer risk. World J Nephrol Urol. 2015;33:1495–1502.
  36. Hrafnkelsdóttir SM, Torfadóttir JE, Aspelund T, et al. Physical activity from early adulthood and risk of prostate cancer: A 24-year follow-up study among icelandic men. Cancer Prev Res. 2015;8(10):905–911.
  37. Clarke G, Whittemore AS. Prostate cancer risk in relation to anthropometry and physical activity: The national health and nutrition examination survey I epidemiological follow-up study. Cancer Epidemiol Biomarkers Prev. 2000;9(9):875–881.
  38. Norman A, Moradi T, Gridley G, et al. Occupational physical activity and risk for prostate cancer in a nationwide cohort study in sweden. Br J Cancer. 2002;86(1):70–75.
  39. Orsini N, Bellocco R, Bottai M, et al. A prospective study of lifetime physical activity and prostate cancer incidence and mortality. Br J Cancer. 2009;101(11):1932–1938.
  40. Parent MÉ, Rousseau MC, El-Zein M, et al. Occupational and recreational physical activity during adult life and the risk of cancer among men. Cancer Epidemiol. 2011;35(2):151–159
  41. Vidarsdottir H, Gunnarsdottir HK, Olafsdottir EJ, et al. Cancer risk by education in iceland; a census-based cohort study. Acta Oncologica. 2008;47(3):385–390.
  42. Doolan GW, Benke G, Giles GG, et al. A case control study investigating the effects of levels of physical activity at work as a risk factor for prostate cancer. Environ Health. 2014;13:64.
  43. Hosseini M, Seyed ASA, Mahmoudi M, et al. A case-control study of risk factors for prostate cancer in iran. Acta medica Iranica. 2010;48(1):61–66.
  44. Lacey Jr JV, Deng J, Dosemeci M, et al. Prostate cancer, benign prostatic hyperplasia and physical activity in Shanghai, China. Int J Epidemiol. 2001;30(2):341–349.
  45. Sass‐Kortsak AM, Purdham JT, Kreiger N, et al. Occupational risk factors for prostate cancer. Am J Ind Med. 2007;50(8):568–576.
  46. Friedenreich C, McGregor S, Courneya K, et al. Case-control study of lifetime total physical activity and prostate cancer risk. Am J Epidemiol. 2004;159(8):740–749.
  47. Lagiou A, Samoli E, Georgila C, et al. Occupational physical activity in relation with prostate cancer and benign prostatic hyperplasia. Eur J Cancer Prev. 2008;17(4):336–339.
  48. Wiklund F, Lageros YT, Chang E, et al. Lifetime total physical activity and prostate cancer risk: A population-based case–control study in sweden. Eur J Epidemiol. 2008;23(11):739–746.
  49. Bairati I, Larouche R, Meyer F, et al. Lifetime occupational physical activity and incidental prostate cancer (canada). Cancer Causes Control. 2000;11(8):759–764.
  50. Krishnadasan A, Kennedy N, Zhao Y, et al. Nested case–control study of occupational physical activity and prostate cancer among workers using a job exposure matrix. Cancer Causes Control. 2008;19(1):107–114.
  51. Pierotti B, Altieri A, Talamini R, et al. Lifetime physical activity and prostate cancer risk. Int J Cancer. 2005;114(4):639–642.
  52. Strom SS, Yamamura Y, Flores‐Sandoval FN, et al. Prostate cancer in Mexican Americans: Identification of risk factors. The prostate. 2008;68(5):563–570.
  53. Villeneuve PJ, Johnson KC, Kreiger N, et al. Risk factors for prostate cancer: Results from the canadian national enhanced cancer surveillance system. Cancer Causes Control. 1999;10(5):355–367.
  54. Crespo CJ, Garcia-Palmieri MR, Smit E, et al. Physical activity and prostate cancer mortality in puerto rican men. J Phys Act Health. 2008;5(6):918–929.
  55. Giovannucci E, Leitzmann M, Spiegelman D, et al. A prospective study of physical activity and prostate cancer in male health professionals. Cancer Res. 1998;58(22):5117–5122.
  56. Lee IM, Sesso HD, Paffenbarger RS. A prospective cohort study of physical activity and body size in relation to prostate cancer risk (United States). Cancer Causes Control. 2001;12(2):187–193.
  57. Littman AJ, Kristal AR, White E. Recreational physical activity and prostate cancer risk (United States). Cancer Causes Control. 2006;17(6):831–841.
  58. Liu S, Lee I-M, Linson P, et al. A prospective study of physical activity and risk of prostate cancer in us physicians. Int J Epidemiol. 2000;29(1):29–35.
  59. Platz EA, Leitzmann MF, Michaud DS, et al. Interrelation of energy intake, body size, and physical activity with prostate cancer in a large prospective cohort study. Cancer res. 2003;63(23):8542–8548.
  60. Giovannucci EL, Liu Y, Leitzmann MF, et al. A prospective study of physical activity and incident and fatal prostate cancer. Arch Intern. 2005;165(9):1005–1010.
  61. Moore SC, Peters TM, Ahn J, et al. Physical activity in relation to total, advanced, and fatal prostate cancer. Cancer Epidemiol Biomarkers Prev. 2008;17(9):2458–2466.
  62. Nilsen TI, Romundstad PR, Vatten LJ. Recreational physical activity and risk of prostate cancer: A prospective population‐based study in norway (the hunt study). Int J Cancer. 2006;119(12):2943–2947.
  63. Patel AV, Rodriguez C, Jacobs EJ, Solomon L, Thun MJ, Calle EE. Recreational physical activity and risk of prostate cancer in a large cohort of us men. Cancer Epidemiol Biomarkers Prev. 2005;14(1):275–279.
  64. Wannamethee S, Shaper A, Walker M. Physical activity and risk of cancer in middle-aged men. Br J Cancer. 2001;85(9):1311–1316.
  65. Chen Y, Chiang C, Lin R, et al. Diet, vegetarian food and prostate carcinoma among men in taiwan. Br J Cancer. 2005;93(9):1057–1061.
  66. Sanderson M, Coker AL, Logan P, et al. Lifestyle and prostate cancer among older african-american and caucasian men in south carolina. Cancer Causes Control. 2004;15(7):647–655.
  67. Darlington GA, Kreiger N, Lightfoot N, et al. Prostate cancer risk and diet, recreational physical activity and cigarette smoking. Chronic Dis Can. 2007;27(4):145–153.
  68. Jian L, Shen ZJ, Lee AH, et al. Moderate physical activity and prostate cancer risk: A case–control study in china. Eur J Epidemiol. 2005;20(2):155–160.
  69. Yu H, Harris RE, Wynder EL. Case‐control study of prostate cancer and socioeconomic factors. The Prostate. 1988;13(4):317–325.
  70. Merrill RM, Perego UA, Heiner SW. Age, lifestyle, health risk indicators, and prostate-specific antigen scores in men participating in the world senior games. Rol Oncol-Semin Ori. 2002;105–109.
  71. Oliveria SA, Trichopoulos D, Blair S. The association between cardiorespiratory fitness and prostate cancer. Med Sci Sports Exerc. 1996;28(1):97–104.
  72. Hållmarker U, James S, Michaëlsson K, et al. Cancer incidence in participants in a long-distance ski race (vasaloppet, sweden) compared to the background population. Eur J Cancer. 2015;51(4):558–568.
  73. Galvão DA, Taaffe DR, Spry N, et al. Exercise preserves physical function in prostate cancer patients with bone metastases. Med Sci Sports Exerc. 2018;50(3):393–399.
  74. Richman EL, Kenfield SA, Stampfer MJ, et al. Physical activity after diagnosis and risk of prostate cancer progression: data from the cancer of the prostate strategic urologic research endeavor. Cancer Res. 2011;71(11):3889–3895.
  75. Barb D, Williams CJ, Neuwirth AK, et al. Adiponectin in relation to malignancies: a review of existing basic research and clinical evidence. Am J Clin Nutr. 2007;86(3):S858–S866.
  76. Haverkamp J, Charbonneau B, Ratliff TL. Prostate inflammation and its potential impact on prostate cancer: a current review. J Cell Biochem. 2008;103(5):1344–1353.
  77. Nicklas BJ, Hsu FC, Brinkley TJ, et al. Exercise training and plasma C-reactive protein and interleukin-6 in elderly people. J Am Geriatr Soc. 2008;56(11):2045–2052.
  78. McCullough DJ, Stabley JN, Siemann DW, et al. Modulation of blood flow, hypoxia, and vascular function in orthotopic prostate tumors during exercise. J Natl Cancer Inst. 2014;106(4):dju036.
  79. Lehrer S, Diamond EJ, Stagger S, et al. Increased serum insulin associated with increased risk of prostate cancer recurrence. Prostate. 2002;50(1):1–3.
  80. Roddam AW, Allen NE, Appleby P, et al. Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies. Ann Intern Med. 2008;149(7):461–71.
  81. Leung PS, Aronson WJ, Ngo TH, et al. Exercise alters the IGF axis in vivo and increases p53 protein in prostate tumor cells in vitro. J Appl Physiol. 2004;96(2):450–454.
  82. Gardner JR, Livingston PM, Fraser SF. Effects of exercise on treatment‐related adverse effects for patients with prostate cancer receiving androgen‐deprivation therapy: a systematic review. J Clin Oncol Off J Am Soc Clin Oncol. 2014;32(4):335– 346.
  83. Hydock DS, Wonders KY, Schneider CM, et al. Androgen deprivation therapy and cardiac function: effects of endurance training. Prostate Cancer Prostatic Dis. 2006;9:392–398.
  84. Severson RK, Nomura AM, Grove J S, et al. A prospective analysis of physical activity and cancer. Am J Epidemiol. 1989;130(3):522–529.
  85. Robertson JD, Maughan RJ, Duthie GG, et al. Increased blood antioxidant systems of runners in response to training load. Clin Sci.1991;80(6):611–618.
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